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Fluoride is the major Cause of Cataract Blindness


Abstract and Figures

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.
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Fluoride is the major Cause of Cataract Blindness
Geoff N Pain
August 2017
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.
Keywords: Alkaline Phosphatase, Anticholinesterase agents, Aphakia, Asteroid Hyalosis, Asthma, Bio-
accumulation, Blindness, Calcification, Cataract, Conjunctivitis, Diabetes, Fluoride, Fluorocarbon, Glaucoma,
Hydroxyapatite, Macular Degeneration, Melatonin, Mortality, Optial Neuritis, Osteosarcoma, Pineal gland, Retina,
Smoking, Uveitis
In Australia it is estimated that 40% of visual impairment is due to Cataract, with over 1,460,400 sufferers aged 55 or
more (31% of that age group) in 2004. In the same year 429,600 Australians aged 55 or more had undergone
cataract surgery, which represents 9.1% of that age group [AIHW 2005]. The risk of falls and bone fractures,
automobile accidents, premature death and the rates of depression and anxiety are elevated in those visually
impaired by cataract [Smith 2016].
Cataract is the leading cause of visual impairment in Australian Aborigines who suffer earlier onset of cataract in
their generally shorter life spans [Landers 2013].
In underdeveloped countries, the incidence of new cases outstrips the surgical capacity, producing a worsening
human and economic burden [Khanna 2012]. Surgical rate is a measure of wealth of nations and surgical failure is
significant, often resulting in aphakia or eye loss.
There are various types of cataract [Gruebbel 2014], however the focus of this review is the highly mineralized
forms, which have been known since 1843 [Jacob 1851] to be due to deposition of needle-like crystals of “phosphate
of lime”, now known as Hydroxyapatite. Calcified cataract is normally age-dependent but has been reported in
young people [Chiang 2004].
Types of Cataract
There are three main types of Cataracts: nuclear; cortical; and subcapsular.
Nuclear cataracts form deep in the central zone of the lens and are usually associated with aging.
Cortical cataracts occur in the lens cortex, the part of the lens that surrounds the central nucleus and have white,
wedge-like opacities that start in the periphery of the lens and work their way to the centre, resembling spokes.
Subcapsular cataract occurs at the back of the lens. People with diabetes or those taking high doses of steroid
medications have a greater risk of developing subcapsular cataracts.
Synchrotron hard X-ray imaging of whole lenses has allowed identification of Calcium in both cortical and nuclear
cataract crystals [Antunes 2006] while other groups using the technique focused on structural change of protein
[Bahrami 2015].
Fluoride doped Hydroxyapatite in Cataract
A study of residents in two towns in Texas with different Fluoride levels in drinking water, Bartlett (8 ppm Fluoride)
and Cameron (0.4 ppm Fluoride) found no statistically significant difference due to small sample size and different
age distributions [Leone 1954]. The National Research Council remarked about this study "The greater incidence in
the high fluoride group (Bartlett) of a certain brittleness and blotching of fingernails, of hypertrophic changes in the
spine and the pelvis, and of lenticular opacities of the eyes (Cataracts) requires further investigation.” [NRC 2006].
Correlation between the incidence of senile cataract and concentration of fluoride in drinking water was observed in
a later studies [Kas’ianenko 1984, Shulka 1991].
Down Syndrome (Mongolism) was established to be linked to consumption of fluoride through statistical studies. It
was found that 70% of Down's Syndrome babies were born with cataract [Rapaport 1957; 1957a; 1959].
Early studies of Fluoride content of Cataract found up to 77 ppm Fluoride [Waldbott 1961].
However humans in Balaghat who drank well water at 1.2-2.4 ppm or river water at 2.8 ppm Fluoride, exhibited
remarkably high levels of 20,000 to 50,000 ppm Fluoride in their removed cataracts [Shulka 1991].
These levels exceed those that have been reported in the Pineal gland and indicate that high levels of Calcium,
Phosphate and Fluoride are available to the lens during cataract formation.
Calcium has been shown to induce opacification and proteolysis in the lens of test animals [Truscott 1990]. Proteases
including calpain I, calpain II, and calpastatin are present in the lens [Yoshida 1985].
Effects of industrial Fluoride exposure in humans include opacities of the lens capsule (cataract) and attenuation of
the retinal arteries [Karczewicz 1989].
Fluoride doped Hydroxyapatite in cataracts and other tissues is less easily resorbed, leading to bio-accumulation and
acceleration of Hydroxyapatite Deposition Disease (HADD). Kidney failure with age, part of which is due to the
nephrotoxicty of Fluoride [Pain 2017], produces an exponential retention of Fluoride and risk of cataract growth.
The European Commission adopted a position on Hydroxyapatite in 2016 stating: “The available information
indicates that nano-hydroxyapatite in needle-shaped form is of concern in relation to potential toxicity. Therefore,
needle-shaped nano-hydroxyapatite should not be used in cosmetic products. It is of note that Material 2 of the
submission also includes nanofibres of needle-like structure.” [EC 2016].
Recently in Australia a famous manufacturer of infant formula was forced to withdraw product from the market due
to discovery of nanocrystals of Fluoride doped Hydroxyapatite in its product [Schoepf 2016, Schoepf 2017,Han
2017]. Energy dispersive x-ray analysis of Hydroxyapatite for Fluoride content can be difficult due to other elements
exhibiting peaks in spectra near 7 kEV.
Crystals of Fluoride doped Hydroxyapatite found in infant formula that was withdrawn from the Australian
market [Schoepf 2016, Han 2017].
Crystals of Fluoride doped Hydroxyapatite grown by use of Silver Diamine Fluoride (above left) [Mei 2017] or by
use of acidulated phosphate fluoride (APF) gel to dissolve human teeth (above right) [Kakei 2012].
Global Incidence of Cataract correlates Fluoride in Drinking Water
Comparison of global Fluoride groundwater contamination with severity of cataract prevalence demonstrates good
correlation where data is available.
In addition to the groundwater, many nations are exposed to additional Fluoride hazard from use of rock salt
containing up to 250 ppm Fluoride and high tea consumption.
Much higher incidence of cataracts is found in most tea-consuming countries such as India, Pakistan, Bangladesh,
Myanmar, People’s Republic of China, and other Southeast Asia.
Cataract is the major cause of blindness in Africa [Steinkuller 1983, Rolfe 1997, WHO 2010].
More detailed mapping of Fluoride groundwater contamination shows that the East Africa Rift suffers the effects of
a long history of volcanic venting rich in Hydrogen Fluoride. It is not surprising therefore that the Fred Hollows
Foundation has chosen to perform its cataract surgery programme in Eritrea, Ethiopia, Kenya, Burundi, Rwanda.
Damage to the Cornea and Retina by Fluoride
It has been known since the 1930s that the Retina is easily damaged by Fluoride [Ashton 1957, Akleyev 2014].
Retinal oedema followed by degenerative changes in 17 out of 94 rabbits occurred within five days of giving sodium
fluoride and the effect was enhanced by fasting [Sorsby 1960]. Studies of the action of Sodium Fluoride in destroying
the Retina suggested that it involved inhibition of enzymes involved in glucose metabolism and ion pumps
[Graymore 1959, Sorsby 1966, Vantsek 1969].
The NHMRC specifically excluded a study finding heavy iridocorneal angle hyperpigmentation and glaucoma
associated with fluorosis [Aytuluner 2002]. Likewise NHMRC excluded a study finding that Fluorinated ocular or
periocular corticosteroids have caused death as well as glaucoma in children [Romano 2003].
The World Health Organization recognizes Fluoride as a cause of Conjunctival Hyperaernia [WHO 2014].
Experimental generation of Cataract with Fluoride in Man and Animals
In just six weeks a man given Sodium Fluoride developed optical neuritis [Geall 1964].
Immersing mammalian eyes in Sodium Fluoride solution generates cataracts in a matter of hours [Hamar 1965].
In the experiment with goat eyes, Lipid peroxide level (LPO), and Protein carbonyl content (PC) were significantly
(p<0.001) increased with the fluoride concentration while glutathione level (GSH) and antioxidant enzymes,
superoxide dismutase (SOD) and catalase (CAT) were significantly decreased [Mishra 2014].
Forty percent of rats given commercially available spring water, containing 100 ppm fluoride, for 24 weeks showed
opacifications, epithelial proliferation, and growth changes, including reduced body weight, lengths of body, femur
and tail, compared to controls [Aytuluner 2003].
Above. In 1954 calf eyes were immersed
in Sodium Fluoride solution to produce
cataracts [Nordmann 1954].
Left. A similar experiment using goat eyes
produced the same result [Mishra 2014].
Hydroxyapatite crystals grow in as well as on interocular lenses
A kinetic study showd that Hydroxyapatite crystals in intraocular lenses can be initiated from their interior through
the development of sufficiently high local supersaturation, realized through the diffusion of calcium and phosphate
ions [Drimtzias 2011]. Carbonate inclusion within hydroxyapatite in both intraocular and human senile cataract was
observed by infrared spectroscopy [Lin 2010]. It is significant that fluorine-surface-modified and unmodified lenses
for implantation in pediatric aphakia were investigated in research excluded from consideration by the NHMRC in
2007 [Thouvenin 1996]. The NHMRC also excluded a study of the mineralization of intraocular lens [Lai 2005].
Hydroxyapatite and Age-related macular degeneration (AMD)
Macula retinopathy and degenerative changes in the retina in relation to Fluoridation were reported in early studies
[Waldbott 1962].
Proof of involvement of Hydroxyapatite in macular degeneration, which involves accumulation of protein and lipid
containing deposits external to the retinal pigment epithelium, was found by examination of cadaver eyes using
electron microscopy and x-ray diffraction [Thompson 2015]. It was observed that the Hydroxyapatite formed
spherules containing amyloid beta (Aβ) peptide or complement factor proteins as well as cholesterol and other
Hydroxyapatite damage to the Eye and Alzheimer’s Disease
The possible link between macular degeneration and Alzheimer’s disease arises from the observation that
Alzheimer’s Aβ-peptide is deposited at sites of complement activation in pathologic deposits associated with aging
and age-related macular degeneration [Johnson 2002]. Fluoride doped Hydroxyapatite is also present in Corpora
Arenacea or “brain sand” [Wilson 2014].
Glaucoma is found five times more frequently in Alzheimer’s disease patients than in aged controls [Bayer 2002].
Calcification of the lens, retina and macular can be assumed, due to reduced light transmission to the
retinohypothalamic tract, to interfere with the Pineal gland melatonin regulating retina suprachiasmatic nucleus axis
which is implicated in aging and Alzheimer’s Disease [Wu 2005].
Accumulation of Fluoride doped Hydroxyapatite is well known in the Pineal gland [Gusek 1983, Alcolado 1986,
Jengelski 1989, Schmid 1993, Luke 1997, Kunz 1998, Kunz 1999, Duffy 2003].
Risk factors for Cataract and related disease involving multiple Fluoride sources
Fluoride in drinking water causes cataract and the effect is dose-dependent. Other risks and associations with
cataract have been identified and are discussed below. The Appendix lists other reported cataract risks.
Table 2. Risk factors and associations with Fluoride for Cataract and related disease
Linked to
Fluoride Link Reference
Fluoride in drinking water
Tea drinking
Waugh 2016; 2017
Heavy Beer drinking
Warnakulasuriya 2002
Styburski 2017,Waugh 2017a
Fluoride in Rock Salt
Smoker Former
Sutton 1986
Smoker Current
Sutton 1986
posterior subcapsular
Bergman 2013
Vandenberg 2012
Diabetes > 10 years
Bergman 2013
Pain 2015c
Blood Glucose level
Pain 2015c
Asthma or Chronic Bronchitis
See Fluorocarbon
Cardiovascular Disease
Pain 2016
Pain 2016
History of Coronary Heart
Pain 2016
Pain 2017b
Fluegge 2016
Diabetes mellitus
Pain 2016
Chlorpromazine > 90 days
High plasma Homocysteine
Medhi 1990, Weiss 2002
Decreased plasma Folate
Ratan 2008, Susheela 2010
Decreased plasma Vitamin B12
Susheela 2010
High glycosylated Haemoglobin
Posterior subcapsular
Susheela 1981
Decreased plasma cholesterol
Wang 1991
Hypothyroidism (Thyroid
Hormone Therapy)
Peckham 2015
Sato 2016
Inhaled Corticosteroids > 5
Valic 1977
Occupational Inhalation
Pre-existing posterior
subcapsular opacities
Asteroid Hyalosis
Hydroxyapatite forms precipitates in the vitreous humor of the eye, sometimes only unilaterally, in the condition
known as Asteroid Hyalosis, previously named Hyalitis [Jervey 1965, March 1975, Winkler 2001, Komatsu 2003,
Kador 2008].
Based on Fluoride analyses available for lens calcification, we can anticipate future research will identify Fluoride in
the mineral content of these “asteroids”.
Diabetes, metabolic disorders and Cataract
Metabolic cataracts include those associated with Diabetes Mellitus, Galactosaemia, Hypercholesteraemia,
Lipidemia, Endocrinological cataract associated with Hypothyroidism and Hypercalcaemia and cataracts associated
with certain skin diseases such as Atopic Dermatitis [Dawson 1981, Kador 2008].
Elevated Plasma albumin, bilirubin, calcium, cortisol, glucose, sodium and γ- glutamyl transpeptidase levels in
cataract patients were linked to liver disease [Donnelly 1995]. Fluoride is a known hepatotoxin.
Diabetes is associated with severe mitochondrial disorders such as Kearns-Sayre syndrome and Mitochondrial
Encephalomyopathy, Lactic Acidosis, and Strokelike episodes (MELAS). Mitochondrial forms of diabetes mellitus
occur in conjunction with hearing loss, myopathy, seizure disorder, strokelike episodes, retinitis pigmentosa,
external ophthalmoplegia and cataracts. There is evidence of maternal inheritance [van den Ouweland 1992,
Khardori 2017]. Increased glycated haemoglobin level was associated with increased risk of nuclear and cortical
cataracts in those with diabetes [Klein 1998]. Fluoride is known to cause Diabetes [Pain 2015c].
Diabetes is associated with low birth weight and while there is a genetic component to low birth weight [Wang
2016], Fluoride is known to cause low birth weight in exposed populations [Hart, MacArthur 2013].
Prevalence studies on diabetes complications reported up to the early 1990s gave widely variable figures. These
have been reviewed in two studies and include figures ranging from 9 to 16 percent for cataract, 7 to 52 percent for
retinopathy, 6 to 47 percent for neuropathy, 6 to 30 percent for nephropathy, and 1 to 5 percent for
macroangiopathy [Mbanya 2003; Rolfe 1997].
Women diabetics suffer higher rates of cataract and earlier surgery than men. Risk factors from the Framingham
heart study that were significantly associated with cataract formation included: elevated blood sugar, elevated blood
pressure, increased serum phospholipids, decreased pulmonary vital capacity, small stature, and less than seven
years of schooling [Kahn 1977].
A patient suffering diabetes, ischemic heart disease, hypertension and renal dysfunction and taking insulin
developed hydroxyapatite cataracts 4 months after implantation of an intraocular lens. Another patient, diabetic and
taking insulin developed hydroxyapatite cataracts 9 months after implantation. Another patient in good overall
health developed hydroxyapatite cataracts 15 months after implantation. All patients received dexamethasone
sodium phosphate eye drops. [Yu 2001].
Cataract and Smoking
Cataracts associated with smoking have been reported to be dose-dependent [Klein 1993, Solberg 1990, West 1995,
Leske 1998, Krishnaiah 2005, Prokofyeva 2013].
Australian data indicated a population attributable risk for smoking and nuclear cataract of 17%, and a risk of 10%
for UV-B exposure and cortical cataract [McCarty 2000, Robman 2005].
Fluorinated Organic Compounds including Drugs and Propellants cause Cataract
Treatment of glaucoma with potent, long-acting anticholinesterase agents including isoflurophate, diisopropyl
fluorophosphates, for 6 months or longer carries high risk of the development of a specific type of cataract, which
begins as anterior subcapsular vacuoles. The incidence of lenticular opacities was as high as 50% with headache,
brow pain, blurred vision, phacodinesis, pericorneal injection, congestive iritis, various allergic reactions, and rarely,
retinal detachment [Gilman 1985, AMA 1983].
Fluorocarbon anaesthetics are known to be metabolized to yield high concentrations of serum Fluoride ion.
Cataract due to the methoxyflurane anaesthetic metabolite calcium oxalate-monohydrate (Whewellite) has been
observed with the pathway for the biotransformation also yielding ionic fluoride [Bullock 1974]. Calcium Oxalate has
also been reported in the lenses of patients with Morgagnian cataracts [Zimmerman 1958].
Drugs used in treatment of asthma are known to cause cataracts, including Flunisolide, Fluticasone Anon
2007].Fluorocarbon propellants used to deliver drugs to patients via “puffers”, including asthma sufferers, are
known to pose serious health hazards due to their metabolism to free Fluoride ion [Silverglade 1972, Valic 1997,
Cumming 1997, Jick 2001]. The observed higher incidence of cataract in users of inhaled drugs is therefore closely
associated with the propellant, often overlooked in epidemiology studies of the drugs in question.
Tetrafluoroethylene has been demonstrated to cause cataracts [NTP 1997].
Flonicamid, an insecticide, causes atrophy of striated muscle fibers, cataract and retinal atrophy observed in the high
dose female rats [Fed Reg 2003]. Fluazifop-p-butyl causes cataracts in 8 out of 12 dogs [Virgo 1982].
Flufenacet, an herbicide has LOEL of 50 ppm [7.4 mg/kg/day] for males 200 ppm [38.4 mg/kg/day] for females based
on cataract incidence and severity [Fed Reg 1998]. Eye effects also included ocular scleral mineralization.
Fluoroquinolones including ciprofloxacin, gatifloxacin, levofloxacin, moxifloxacin, norfloxacin, and ofloxacin cause
uveitis [Wefers Bettink-Remeijer 2009, Butler 2012, Hinkle 2012, Eadie 2014].
Voriconazole increases serum Fluoride to damaging levels. Among the numerous harms caused by this drug are
colour vision change, persistent or severe blurred vision or sensitivity to light.
Visual hallucinations have been found associated with use of fluoxetine and other selective serotonin reuptake
inhibitors [Bourgeois 1998, Schuld 2000].
Fluorinated corticosteroids cause death as well as glaucoma in children [Romano 2003].
Cataract association with Cancer
As previously reviewed, Fluoride doped Hydroxyapatite has been shown to cause malignant cancer of the Breast and
Thyroid [Pain 2015].
In Taiwan, an increased incidence of breast, liver, and head and neck cancers was observed in patients presenting
with Early Onset Cataract [Chiang 2014].
Breast cancer associated with cataracts has also been observed in India [Faridi 2017].
Reactive oxygen species lead to lens opacification through oxidative damage to lens proteins. Increased incidence of
cataract is found in subjects with the null genotype of Glutathione S-Transferase M1 subtype (GSTM1) (odds ratio-
1.51; p<0.05) [Saadat 2012]. The polymorphisms of GSTM1, GSTT1, GSTP1 and GSTO2 have been shown to be
associated with increased risk of developing breast cancer [Sohail 2013]. Raised serum sialic acid, caused by Fluoride
[Needham 2010], is found associated with both cataract and Osteosarcoma [Sandhu 2011].
Cataract association with increased risk of Death
In non-diabetic women the age adjusted cataract mortality hazard ratios were: nuclear opacity (1.8), cortical opacity
(1.9), and posterior subcapsular opacity (2.1). There was no significant difference in mortality risk for men. Among
diabetics, the mortality was significantly higher in both men and women with cataract with age and sex adjusted
hazard ratio of 2.6 [Reidy 2002].
Other mortality studies have been contradictory. When confined to nuclear cataract, there appears to be a more
consistent trend across studies with 11 out of 15 showing significantly increased risk of death. Unfortunately many
studies do not distinguish the type of cataract and few refer to calcification [Khanna 2013].
Nuclear opacity (RR, 1.40; 95% CI, 1.121.75) and cataract surgery (RR, 1.55; 95% CI, 1.182.05) were associated with
increased all-cause mortality and with cancer deaths [Clemons 2004].
Higher risks were found for black Barbados residents with cumulative 4-year mortality varied with lens types,
increasing from 3.2% for those without cataract to 6.0% for cortical-only, 8.8% for nuclear-only, and 20.9% for mixed
opacities. Coexisting diabetes further increased mortality: people with mixed opacities and diabetes had a 2.7-fold
increased risk of death [Hennis 2001].
Mechanisms of Fluoride induced Cataract
The toxic effects of fluoride in the eye appear to follow universal mechanisms found in a wide variety of cells
[Barbier 2010, Agalakova 2012].
The mechanisms of fluoride toxicity can be summarized [Pain 2017a] under the following headings:
Mutation and abnormal embryo development with altered expression
Endocrine disruption
Altered enzyme levels and enzyme inhibition
Oxidative stress with generation of reactive oxygen species and radicals
Apoptosis via mitochondria mediated and Caspase dependent pathways
Disruption of ion channels affecting pH, cation and anion balance
Physical damage from calcification
Fluoride Disrupts Phosphate Pathways
Metabolic disturbance, chronic hypocalcemia and hyperphosphatemia, calcitonin reduction, vitamin D insufficiency
can be responsible for cataract formation [Stein 1980, Ogiso 1990, Brown 2015].
Elevated phosphate levels have been measured in the aqueous humor of cataract patients compared to glaucoma
patients. Variation of various phosphatase levels were also found [Latarya 2012].
Cataract calcification will of course be facilitated by elevated phosphate via enhanced crystal growth of Fluoride
doped Hydroxyapatite.
Measurement of Alkaline phosphatase is often used to detect systemic toxic reaction as it is an indicator of abnormal
bone turnover and hepatobiliary diseases [Mallik 2016].
Alkaline phosphatase (10.6%), acid phosphatase (24.09%) increased in brains of mice after administration of sodium
Fluoride [Reddy 2009].
Fluoride inhibits acid phosphatases (protein phosphoseryl and phosphothreonyl phosphatases or PSPs), which are
necessary for the phosphorylation of glucose, adenosine triphosphatase, and enolase, the enzyme responsible for
the formation of phosphopyruvic acid from 2-phosphoglyceric acid [Nordmann 1954]. Sodium Fluoride is sold as a
reagent of choice to irreversibly inhibit Acid Phosphatases [Thermo Fisher Scientific 2017].
Mechanistic studies identify Fluoride attack on the metal ion centres in acid phosphatases, notably Iron and Zinc,
preventing coordination of water molecules essential for their function [Pinske 1999, Srivastava 2015].
Acid phosphatase and lipid peroxidation have been measured in human cataractous lens epithelium. Lipid
peroxidation in mature cataractous lens epithelium was correlated with increased permeability of the plasma
membrane [Vasavada 1993].
Fluoride inhibition of acid phosphatase is also related to male infertility [Nag Das 1984] and prostate disease [Reiner
Congenital Cataracts Facial Dysmorphism Neuropathy Syndrome involves a single-nucleotide substitution producing
a nonfunctional protein in formation of Fcp1 which is the main serine phosphatase for the C-terminal domain of
eukaryotic RNA polymerase II, which regulates transcription by recruiting different factors to nascent mRNA [Varon
Alkaline phosphatase, elevated in cataract patients [Donnelly 1995, Fernandes 2011], is also greatly increased in
osteosarcoma, a neoplastic proliferation of osteoblasts [Krook 1998].
Alkaline Phosphatase is an enzyme which catalyses the hydrolysis of a number of phosphate esters, transferring the
phosphate group to an acceptor molecule. Fluoride has been shown to increase serum alkaline phosphatase that
results in increased deposition of Hydroxyapatite [Farley 1983, Khokher 1990, Shanthakumari 2004, Fernandes
2011]. Chronic industrial airborne Fluoride exposure increased worker serum alkaline phosphatase (ALP) and
superoxide dismutase (SOD).
Raised levels of alkaline phosphatase induce hypocalcemia, which triggers parathyroid hyperactivity [Krook 1998].
Hypoparathyroidism is an uncommon condition characterized by spontaneously lowered synthesis and/or secretion
of parathyroid hormone (PTH), which results in profound hypocalcemia and hyperphosphatemia [Liao 2016]. It is a
result of prevention of calcium reabsorption in renal tubulus and bone matrix, as well as insufficiency of the
synthesis of 1,25- dihydroxyvitamin D3 [1,25(OH)2D3] from its inactive precursor 25- hydroxyvitamin D.
Fluoride induces cell injury in both osteoblasts and osteocytes, initiating a repair response that results in increased
alkaline phosphatase [Krook 1998]. An increase of serum alkaline phosphatase results in enhanced hydroxyapatite
deposition measured as increased bone mass following fluoride dosing. Unfortunately, it seems little attention has
been paid to the more difficult task of measuring the enhanced deposition of hydroxyapatite in soft tissues.
Alkaline phosphatase is inhibited by Fluoride in the gut of the silkworm [Miao 2005].
Rats treated with Fluoride in drinking water for 90 days show high serum alkaline phosphatase accompanied by
hypocalcemia and hyerphosphatemia [Gupta 2016].
Fluoride causes Oxidative Stress leading to Cataracts
Lipid peroxidation is known to cause cataracts from research that was specifically excluded from consideration by
the NHMRC in 2007 [Babizhayev 2004]. Further research by the same group found that oxidative stress in
mitochondria induces generation of reactive oxygen species (ROS) and redox imbalance of the eye lens leading to
human cataract formation with formation of phospholipid hydroperoxides as a common basis for cataract disease
[Babizhayev 2011].
Various oxidative stress markers have been studied in human cataract patients [Sawada 2009, Tomar 2014]. A study
in Jaipur, India, compared randomly selected patients with cataract from a high Fluoride region, ground water F>2.5
ppm, with age- and sex-matched control patients with cataract from a low-fluoride region, ground water F<1.5 ppm
[Tomar 2014]. Oxidative stress markers studied were Lipid peroxide levels (LPO), protein carbonylation (PC),
superoxide dismutase (SOD), catalase (CAT), and glutathione (GSH), serum F estimations, and the measurement of
trace metallevels (Cu, Zn, Se, and Fe). Significantly higher LPO and PC were found in the high-F region subjects in
both serum and lenses. Antioxidant enzyme SOD and GSH were found to be markedly decreased in the blood and
lenses of the high-F region subjects [Tomar 2014].
Methylglyoxal is implicated in cataract development by inducing endoplasmic reticulum stress in human lens
epithelial cells, and activating an unfolded protein response leading to overproduction of ROS and altering the
cellular redox balance toward lens oxidation [Palsamy 2014].
Sialic acid, is a marker for inflammation and oxidative stress and is released from the terminal oligosaccharide chain
of some glycoproteins and glycolipids. Cataract is associated with the increase in serum sialic acid level [Mallik 2016].
Fluoride is known to increase sialic acid levels [Susheela 1982].
Gamma glutamyl transpeptidase is another marker for oxidative stress that is elevated in cataract as well as liver and
cardiovascular disease [Emdin 2005, Mallik 2016].
Fluoride Disrupts Ion Transport
As discussed above, Fluoride disrupts the anaerobic metabolic pathways which provide the energy for ion transport.
The lens excretes sodium and concentrates potassium in cataracts [Mallik 2016].
Elevated magnesium was found in the serum of cataract patients [Ringvold 1988].
Light damages cation pump activity via superoxide formation, attenuated by ascorbate in the aqueous humour
[Varma 1984].
Alteration in ion transport can lead to variation in hydration of the lens, leading to myopia and glaucoma.
Attempted amelioration of Cataract
Antioxidant vitamin supplements have been investigated as a means of slowing, if not preventing, eye disease
including cataract and macular degeneration.
Vitamin E showed some promise in one study [Vitale 1993] but proved a risk factor in another [McCarty 2000].
It has been suggested that in Turkey, with the maximum per capita use of tea in the world, supplying up to 376 mg of
caffeine per day, that the antioxidant properties of caffeine might lower incidence of cataract [Varma 2016].
Evidence that is consistent with Fluoride inhibition of metallo-enzymes is the observation that Zinc supplements
provide a protective effect [Clemons 2004].
Salicylates lower plasma levels of tryptophan and prevent binding to the lens, significantly retarding UV cataract
formation in both diabetics and non-diabetics.
Significantly lower incidences of nuclear cataracts 5 years later occurred in those who took thiazide diuretics
(OR=0.79, 95% CI 0.63, 1.00) and aspirin (OR=0.76, 95% CI 0.61, 0.95) at the baseline examination [Klein 2001] with
the aspirin result contradicting increased risk found elsewhere [Christen 2001].
The only safe place for Hydroxyapatite storage is in bone. When deposited in the soft tissues, it resembles asbestos,
causing numerous diseases including those leading to blindness and premature death.
Fluoride doping exacerbates this calcification and every effort must be made to reduce Fluoride exposure in the
diet. The deliberate addition of Fluoride to milk or salt is reckless.
Elimination of deliberate water Fluoridation programmes and defluoridation of contaminated groundwater will
greatly reduce the global burden of preventable eye disease.
Fluoride contribution to incidence of age-related macular degeneration, diabetic retinopathy, glaucoma and a
proportion of “undetermined cause” global blindness should be recognized in epidemiology studies and future plans
to remedy the suffering.
The World Health Organization should update its warnings about Fluoride as a chemical of concern with added
emphasis on loss of vision so that the few remaining countries that have not banned water Fluoridation will have
extra incentive to act [WHO 2010;2014].
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Appendix: Risk factors for Cataract other than Fluoride
Risk factors for Cataract include physical injury to the eye, exposure to solar radiation (UV-B), intense heat and
dehydration, rare genetic disorders and dietary supplements, not discussed in any detail here.
Below is a brief tabulation of references that discuss identified risk factors for cataract that do not involve Fluoride.
However it is worth noting that some multivitamin preparations do contain deliberately added Fluoride, despite the
USFDA ban on the practice.
Table 1. Cataract Risk Factors not Associated with Fluoride
Risk Factor
Family History of Cataract
Leske 1998
Multivitamin ⁄ Mineral supplements
Maraini 2008
David 1984, Hightower
1987, Mishra 2013
Vitamin C
Rautiainen 2010
Valero 2002
Solar, UVB radiation, X-rays
Hollows 1981
Dawson 1981
Dexamethasone sodium phosphate
eye drops
Yu 2001
Shui 2009
Australian Aboriginal
Randall 2014
1.1 - 1.5
Chang 2001,
Laitinen 2009
Genetic Predisposition
UVB radiation
Hollows 1981
Ambient Temperature
Sasaki 2002
Latitude (light intensity)
Javitt 1994
Bone Marrow Transplantation
Aristei 2002
Measles, Mumps and Rubella
Ferrini 2013
Anti-Hypertensive drugs
Younan 2003
Gout medications, Allopurinol
Leske 1998
Vitamin E
McCarty 2000
Cumming 1998,
Christen 2001
Klein 2001
Oral hypoglycaemic agents
Klein 2001
Klein 2001
The cataracts associated with bone marrow transplantation are thought to be caused by the radiation [Aristei 2002].
X-rays were noted to induce cataracts in human subjects during the first two decades of the 20th century.
Solar radiation and especially its Ultraviolet component produces significantly more cataracts in people over 65 years
of age living in regions with more hours of sunshine. Comparison of human lenses removed for cataract in Rochester,
New York, Tampa, Florida, and Manila, The Philippines revealed a significant correlation between the prevalence of
black cataracts, proximity to the equator, and outdoor occupation.
Black or brown cataracts are different to mineralized cataracts and exhibit damage to protein and organic structure
and are formed of brown pigments from tryptophan (significantly elevated in UV cataract patients) and free radical
cross-linking of lens proteins in the absence of adequate sulfhydryl groups in glutathione. Tryptophan and its
metabolite, kynurenine, bind to lens protein.
Young children with the inborn error of metabolism, galactosaemia, develop cataract as part of this fatal disorder. It
has been postulated that the excess galactose is metabolized by aldose reductase to dulcitol, which accumulates in
the lens and leads to cataract formation. Similarly, it has been shown that male subjects who lack glucose-6-
phosphate dehydrogenase in their red blood cells have an increased rate of presenile cataract formation in adult life
[Dawson 1981].
Calcium-activated proteolysis has been studied in the lens nucleus during selenite cataractogenesis [David 1984,
Hightower 1987, Mishra 2013].
... Because Fluoride is a universal toxin that damages all types of mammalian cells, the list of harms from drinking Green Tea will follow those observed by Fluoride from drinking water [Pain 2017a] including cataract blindness [Pain 2017b]. The following discussion covers harms so far identified arising through drinking of Green Tea. ...
Technical Report
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Green Tea is promoted as a healthy beverage yet few consumers are aware of the health risks caused by its Aluminium, Fluoride, Fluoroacetate, Heavy Metal, Oxalate and Polyphenol content.
... Comorbidity studies are proving useful as shown by correlation between Fluorosis and Cataract [Pain 2017b]. ...
Technical Report
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The people of Port Macquarie Hastings in the state New South Wales, Australia, voted overwhelmingly against Fluoridation of their drinking water but their wishes were ignored due to political pressure to aid the disposal of industrial waste from the Phosphate Fertilizer industry. The water supply is drawn from the Hastings River and the project is unusual due to storage of unfiltered Fluoridated water in interconnected earth dams exposed to sunlight. No environmental impact assessment was performed before the project despite the presence of threatened, vulnerable and endangered wildlife in the catchment area. Risks to public health from organic molecules containing Fluorine manufactured by bacteria and algae appear never to have been considered.
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.
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Excessive fluoride intoxication plays an important role in the development of dental, skeletal and non-skeletal fluorosis. The aim of this study was to ascertain the toxic effect of excessive fluoride ingestion on the level of hydroxyproline and expression of type 1 collagen gene in rat bone and its amelioration by supplementation with Tamarindus indica fruit pulp extract. Forty albino rats were randomly assigned to four groups. The first group served as control and received only tap water. The second group received sodium fluoride (200 ppm) through drinking water. The third group received T. indica fruit pulp extract (200 mg/kg body weight) alone and the fourth group received the T. indica fruit pulp extract (200 mg/kg body weight) along with fluorinated drinking water (200 ppm) daily by gavage for a period of 90 days. The level of hydroxyproline and expression of type 1 collagen gene using quantitative real time PCR in the tibia bone decreased significantly with continuous exposure to sodium fluoride. Co-administration of T. indica fruit pulp extract during exposure to fluoride through drinking water restored the level of calcium, phosphorus and alkaline phosphatase in serum and the concentration of hydroxyproline in urine. It increased the level of hydroxyproline and expression of type 1 collagen gene in the tibia as compared to untreated fluoride-exposed rats. It is concluded that T. indica fruit pulp extract has an ameliorative potential to protect the bone from fluoride induced collagen damage.
Full-text available
A recent nation-wide population based retrospective cohort study from Taiwan in 2014 suggested a propensity of developing breast cancer in young females with early-onset cataract. We report here a case of a young non-obese female who presented to us with a large lump in the right breast with skin nodules and bilateral painless progressive diminution of vision. Patient was diagnosed to be suffering from locally advanced carcinoma of right breast with axillary metastasis (Stage III B) and bilateral early-onset nuclear cataract. Patient was started on taxane and anthracycline based neoadjuvant chemotherapy and after three cycles of chemotherapy patient showed partial response (≈50% reduction of tumour mass). Patient underwent small incision cataract surgery in left eye after the first cycle of chemotherapy. However, the patient was lost before any operative intervention could be done as she died in a road traffic accident. Possible mechanism of development of breast cancer in patients with early-onset cataract is discussed. This is the first reported case of a patient of early–onset cataract developing breast cancer as well as the first reported case of concomitant presence of early-onset bilateral cataract with breast cancer.
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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.
Diabetes is a chronic condition that afflicts over 450 million people worldwide. Diabetes can lead to the development of multiple chronic comorbidities, such as microvascular, macrovascular, and neuropathic complications. Furthermore, diabetes is the leading cause for many of these complications, such as blindness, peripheral arterial disease, and kidney disease. Many of these conditions can go unnoticed for many years until they become more severe and are no longer reversible. This article will provide an evidence-based review of the background, prevention, and screening for many of the complications of diabetes.
The levels of sialic acid and glycosaminoglycans (GAG) have been explored in the serum of fluoresced human subjects. The changes observed in the level of these chemical constituents in the serum possibly reflect the changes occurring in cancellous bone, cortical bone and in other tissues due to fluoride ingestion. The sialic acid content versus GAG revealed a 50% reduction in serum from fluorosed subjects. The possibility of developing a sensitive prognostic test for fluorosis is discussed.
Silver diamine fluoride (SDF) is found to promote remineralization and harden the carious lesion. Hydroxyapatite crystallization is a crucial process in remineralization; however, the role of SDF in crystal formation is unknown. We designed an in vitro experiment with calcium phosphate with different SDF concentrations (0.38, 1.52, 2.66, 3.80 mg/mL) to investigate the effect of this additive on the nucleation and growth of apatite crystals. Two control groups were also prepared-calcium phosphate (CaCl2·2H2O + K2HPO4 in buffer solution) and SDF (Ag[NH3]2F in buffer solution). After incubation at 37 (o)C for 24 h, the shape and organization of the crystals were examined by bright-field transmission electron microscopy and electron diffraction. Unit cell parameters of the obtained crystals were determined with powder X-ray diffraction. The vibrational and rotational modes of phosphate groups were analyzed with Raman microscopy. The transmission electron microscopy and selected-area electron diffraction confirmed that all solids precipitated within the SDF groups were crystalline and that there was a positive correlation between the increased percentage of crystal size and the concentration of SDF. The powder X-ray diffraction patterns indicated that fluorohydroxyapatite and silver chloride were formed in all the SDF groups. Compared with calcium phosphate control, a contraction of the unit cell in the a-direction but not the c-direction in SDF groups was revealed, which suggested that small localized fluoride anions substituted the hydroxyl anions in hydroxyapatite crystals. This was further evidenced by the Raman spectra, which displayed up-field shift of the phosphate band in all the SDF groups and confirmed that the chemical environment of the phosphate functionalities indeed changed. The results suggested that SDF reacted with calcium and phosphate ions and produced fluorohydroxyapatite. This preferential precipitation of fluorohydroxyapatite with reduced solubility could be one of the main factors for arrest of caries lesions treated with SDF.
The unknowns surrounding presence, composition and transformations during the use phase of engineered nanoparticles (ENPs) in consumer products raises potential human and environmental health concerns and public discourse. This research developed evidence and confirmatory analytical methods to determine the presence and composition of ENPs in a consumer product with a complex organic matrix (six different infant formula samples). Nano-scale crystalline needle-shaped hydroxyapatite (HA; appx. 25 nm × 150 nm) primary particles, present as aggregates (0.3–2 μm), were detected in half the samples. This is the first report of these ENPs in infant formula. Dissolution experiments with needle-shaped HA were conducted to assess potential transformations of nano-HA particles. Rapid dissolution of needle-shaped HA occurred only under lower pH conditions present in simulated biological fluids (acidic gastric fluids), but not in simulated drinking water (near-neutral pH). Other non-nanosized HA minerals exhibited less dissolution under the same low pH conditions. This work demonstrates the occurrence of engineered nanomaterials in the food supply of a sensitive population (infants) and the need to consider transformations in nanomaterials that occur during use, which result in different exposures between pristine/as-produced ENPs and nanomaterials after passing through the human gut.