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Hi Amy,

There are specific water filters made just to remove the fluoride from our

water. Fluoride is NOT good--it's toxic and used to be used as RAT

poison!!! Fluoride is linked to a severe form of childhood and teenage

cancer in boys (I'll see if I can find the reference for this). Fluoride

actually causes MORE tooth decay!!! Fluoride was grandfathered in (it was

NOT checked for toxicity) because it was already in use as rat poison

before the FDA rules regarding testing drugs were put into effect. In

short, your dentist is misinformed.

There is widespread acceptance for purposely avoiding fluoride among both

the autism community, and individuals interested in healthy living. You

will notice that a lot of the toothpaste at health food stores if

fluoride-free. I'll see if I can find you some more articles about

this. Remember, dentists are the same people that put amalgams containing

mercury in our teeth!!!!!!!!!!!!!!!!!!!!!!!!!! Dentists take an oath

preventing them from advising us to get our amalgams

out. UNBELIEVABLE!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!

At 04:38 AM 9/3/2005 -0700, you wrote:

>Hi everyone:

>

>My ASD son uses non fluoride toothpaste. I just

>visited a pediatric dentist for his first check up and

>he was really concerned that my son doesn't get any

>fluoride. I explained to him about trying to reduce

>his toxic load based on his metals test and that he

>gets no chemicals or artificial anything.

>

>He did understand this and knows some of patients who

>are chelating. (he's a special needs dentist)

>However, he said of all the patients he

>knows...fluoride was never a problem.

>

>He said that for my sons permanent teeth he needs the

>fluoride to keep the enamel strong and to of course,

>keep the teeth from decaying.

>

>Any thoughts on the importance of fluoride for our

>kids? Isn't there any " natural " way to prevent

>cavities and make teeth strong at the same time?

>

>thanks. Amy

>

>

>

>____________________________________________________

>Start your day with - make it your home page

><http://www./r/hs>http://www./r/hs

>

>

>

>

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My little brother died of osteosarcoma when he was 14 due to high

fluoride in our municipal water (in So. Cal).

THE OBSERVER , LONDON

Monday, Jun 13, 2005,Page 6

Fluoride in tap water can cause bone cancer in boys, a disturbing new

study indicates, although there is no evidence of a link for girls.

New US research suggests that boys exposed to fluoride between the

ages of five and 10 will suffer an increased rate of osteosarcoma --

bone cancer -- between the ages of 10 and 19.

In the UK, fluoride is added to tap water on the advice of bodies

such as the British Dental Association. The Department of Health

maintains that it is a cost-effective public health measure that

helps prevent tooth decay in children.

The increased cancer risks, identified in a newly available study

conducted at the Harvard School of Dental Health, were found at

fluoride exposure levels common in the US and other countries. It was

the first examination of the link between exposure to the chemical at

the critical period of a child's development and the age of onset of

bone cancer.

Although osteosarcoma is rare, accounting for only about 3 percent of

childhood cancers, it is especially dangerous. The mortality rate in

the first five years is about 50 percent, and nearly all survivors

have limbs amputated, usually legs.

The research has been made available by the Environmental Working

Group (EWG), a respected Washington-based research organization. The

group reports that it has assembled a " strong body of peer-reviewed

evidence " and has asked that fluoride in tap water be added to the US

government's classified list of substances known or anticipated to

cause cancer in humans.

" This is a very specific cancer in a defined population of children, "

said Wiles, the group's co-founder.

" When you focus in and look for the incidence of tumors, you see the

increase. We recognize the potential benefits of fluoride to dental

health, " Wiles said, " but I've spent 20 years in public health,

trying to protect kids from toxic exposure. Even with DDT, you don't

have the consistently strong data that the compound can cause cancer

as you now have with fluoride. "

Half of all fluoride ingested is stored in the body, accumulating in

calcifying tissue such as teeth and bones and in the pineal gland in

the brain, although more than 90 percent is taken into the bones.

Anti-fluoride campaigners argue that the whole issue has become

highly politically sensitive. If health scares about fluoride were to

be recognized in the courts, the litigation, especially in the US,

could be expected to run for decades. Consequently, scientists have

been inhibited from publicizing any adverse findings.

The new evidence only emerged by a circuitous process. It was

contained in a Harvard dissertation by Dr Elise Bassin at the Harvard

School of Dental Medicine. The dissertation, completed in April 2001,

obviously had merit because Bassin was awarded her doctorate.

However it has not been published. Environmental organizations were

repeatedly denied access to it, and even bodies such as the US

National Academy of Sciences could not get hold of a copy. Eventually

two researchers from the Fluoride Action Network were allowed to read

it in the rare books and special collections room at Harvard medical

library.

On Sep 3, 2005, at 6:52 AM, R. Owen wrote:

> Fluoride is linked to a severe form of childhood and teenage

> cancer in boys (I'll see if I can find the reference for this).

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When my middle son was a baby, his doctor switched him at three months to

Poly-Vi-

Fluor vitamins instead of Poly-Vi-Sol...only difference, new vitamin contained

fluoride.

Immediately he developed a chloracne type-rash and even got a sebaceous cyst on

his

cheek which had to be surgically removed. This alerted me to the fact that

fluoride

sensitivities were present in my family, and I discovered that large cysts on my

own chin

which came up and often became infected were only present when I used fluoride

toothpaste. My daughter gets the same kind of reaction. It is HARD to find

fluoride-free

toothpaste sometimes, outside of a health food store. I use Desert Essence tea

tree oil

kind. When I had a support group for interstitial cystitis patients in upstate

NY, one

woman had blood tests to determine what delayed (IgG) reactions she had, and the

main

allergy that was causing her severe bladder pain was fluoride in the water.

Another friend

was disabled as a child from juvenile arthritis that only came up when they

moved into a

county with fluoridated water (in NYC I believe), and recovered after she got

away from it. I

would be tempted to go tell the dentist to go peddle his poisons somewhere else.

Peace,

Kathy E.

> Hi Amy,

>

> There are specific water filters made just to remove the fluoride from our

> water. Fluoride is NOT good--it's toxic and used to be used as RAT

> poison!!! Fluoride is linked to a severe form of childhood and teenage

> cancer in boys (I'll see if I can find the reference for this). Fluoride

> actually causes MORE tooth decay!!! Fluoride was grandfathered in (it was

> NOT checked for toxicity) because it was already in use as rat poison

> before the FDA rules regarding testing drugs were put into effect. In

> short, your dentist is misinformed.

>

> There is widespread acceptance for purposely avoiding fluoride among both

> the autism community, and individuals interested in healthy living. You

> will notice that a lot of the toothpaste at health food stores if

> fluoride-free. I'll see if I can find you some more articles about

> this.

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Hi:

Flouride is a neurotoxin.

It's great your dentist is sensitive to toxicity in general but perhaps he

doesn't know that fluoride has been shown to INCREASE the toxicity of other

toxins like aluminum.

Am scrambling today - as every day these days - and don't have time to post

everything I have but was able to pull this last one up quickly.

BTW - Thanks to everyone who responded to my diarrhea question. I like the

macaroon suggestion the bestbut didn't get a chance to try it.

Josie

___________________________________________________________________

Fluoride 2004;37(4):301-314 Research Review 301

Fluoride 2004;37(4)

Dr Blaylock, a Board-certified neurosurgeon, Visiting Professor of Biology

at Belhaven College,

, Mississippi, and member of the Editorial Board of the Journal of

the American

Nutraceutical Association (JANA), is the author of three books on

excitotoxicity: Excitoxicity: the

taste that kills, Health and nutrition secrets, and Natural strategies for

cancer patients.

EXCITOTOXICITY: A POSSIBLE CENTRAL MECHANISM IN

FLUORIDE NEUROTOXICITY

L Blaylocka

Ridgeland, MS, USA

SUMMARY: Recent evidence indicates that fluoride produces neuronal

destruction

and synaptic injury by a mechanism that involves free radical production and

lipid

peroxidation. For a number of pathological disorders of the central nervous

system

(CNS), excitotoxicity plays a critical role. Various studies have shown that

many of

the neurotoxic metals, such as mercury, lead, aluminum, and iron also injure

neural

elements in the CNS by an excitotoxic mechanism. Free radical generation and

lipid

peroxidation, especially in the face of hypomagnesemia and low neuronal

energy

production, also magnify excitotoxic sensitivity of neurons and their

elements. This

paper reviews briefly some of the studies that point to a common mechanism

for the

CNS neurotoxic effects of fluoride and calls for research directed toward

further

elucidation of this mechanism.

Keywords: Aspartate; Excitotoxicity; Fluoride neurotoxicity; Fluoroaluminum

complexes;

Glutamate; 4-Hydroxynonenal; Melatonin; Neurodegeneration; Peroxynitrite;

Reactive nitrogen

species; Reactive oxygen species.

INTRODUCTION

Compelling evidence indicates that fluoride produces injury to the central

nervous

system (CNS) by several mechanisms. Of particular interest is the ability of

fluoride to induce free radical generation and lipid peroxidation in the

brain,

especially in the hippocampus. In addition, fluoride enhances aluminum

absorption

from the gastrointestinal mucosa and across the blood-brain barrier. Of

particular

concern is the recent demonstration that fluoride readily forms a chemical

complex with aluminum, similar to the phosphate ion, which is toxic to

neurons

at low concentrations and can act as an activator of G-proteins, a membrane

link

to second messenger activation.

While it appears that the toxicity of fluoride is secondary to many widely

divergent

and unrelated processes, there is compelling evidence that a central

mechanism

may be involved called excitotoxicity (Figure and Table).

aFor correspondence: L Blaylock, MD, 315 Rolling Meadows Road,

Ridgeland, MS

39157, USA. E-mail: blay6307@...

302 Blaylock

Fluoride 2004;37(4)

Figure. Possible mechanisms for neurodegenerative effects of fluoride and

aluminum as

related to excitotoxicity. The broken arrow represents the effects of both

elements.

In a recent series of papers, I argue that excitotoxicity is also the

central mechanism

of autism and the Gulf War Syndrome.2-4

The process involves accumulation of acidic amino acids in the synaptic

cleft

Figure. Possible mechanisms for neurodegenerative effects of fluoride and

aluminum as

related to excitotoxicity. The broken arrow represents the effects of both

elements.

WHAT IS EXCITOTOXICITY?

Excitotoxicity is a common mechanism seen in many neurological disorders,

including strokes, brain trauma, CNS infections, autoimmune disorders,

multiple

sclerosis, heavy metal toxicity, brain tumors, and the majority of

neurodegenerative

diseases, such as Alzheimer's dementia, Parkinson's disease, and Lou

Gehrig's

disease (amyotrophic lateral sclerosis, ALS).1 In a recent series of papers,

I

argue that excitotoxicity is also the central mechanism of autism and the

Gulf

War Syndrome.2-4

Fluoride

Aluminum

Microglial

Activation

Impair

transp

Reactive oxygen species and

reactive nitrogen species/

Lipid peroxidation products

(4-HNE)

Reduced

GSHPx,G

Excitoxicity: a possible central mechanism in fluoride neurotoxicity 303

Fluoride 2004;37(4)

The process involves accumulation of acidic amino acids in the synaptic

cleft

for a prolonged period. These special amino acids include cysteine, cysteine

sulfinic acid, cysteic acid, and homocysteine, as well as the

neurotransmitters

glutamate and aspartate. The neurotransmitters glutamate and aspartate

normally

activate a series of glutamate receptors on the postsynaptic membrane that

leads

to neuronal excitation. In fact, glutamate is the most abundant

neurotransmitter in

the CNS and is responsible for attention, alertness, and learning. It is

also the

most neurotoxic.

If the excitatory amino acids are not removed quickly from the synaptic

cleft,

the postsynaptic neurons become overstimulated, leading to either synaptic

destruction and dendritic retraction or, should the stimulation be prolonged

and

intense, neuronal destruction by both apoptosis and necrosis.5 It is for

these reasons

that extracellular glutamate levels are carefully regulated by a series of

glutamate transporters, which remove the glutamate for storage, either in

the presynaptic

neuron terminal or surrounding astrocytes (glia).6

Table. Comparison of the effects of fluoride/aluminium and excitotoxicity

Fluoride/Aluminium Excitotoxicity

Increased brain reactive oxygen species (ROS)

and reactive nitrogen species (RNS)

yes yes

Increased lipid peroxidation (LPO) yes yes

Decreased glutathione yes yes

Decreased superoxide dismutase (SOD) yes yes

Elevated brain ascorbate yes yes

Hippocampal apoptosis necrosis yes yes

G-protein activation yes yes

Synaptic injury yes yes

Impaired glutamate uptake yes yes

Microglial activation ? for fluoride

yes for aluminium

yes

ROS in other tissues ? for fluoride

yes for aluminium

yes

DNA injury yes yes

304 Blaylock

Fluoride 2004;37(4)

This excitotoxic process was originally discovered by two ophthalmologists,

Lucas and Newhouse in 19577 and given the name excitotoxicity by Dr

Olney in 1969.8 Since its discovery, a great deal has been learned about the

mechanism

of excitotoxicity, the receptors involved, and the glutamate uptake system.

In addition, much has been discovered about other toxins that can activate

this

destructive process. Recently, glutamate receptors have been found in

numerous

peripheral tissues, including the testes, lungs, pancreatic islet cells,

cardiac

nerves, ovaries, endothelial cells, immune cells, and bone osteoblasts.9

COMMON MECHANISMS

1.Free radical generation

Glutamate receptors are found in numerous types of neurons, including those

that utilize other neurotransmitters, such as GABA (gamma-aminobutyric

acid),

dopamine, norepinephrine, and serotonin.10 There are two basic types of

glutamate receptors, ion-gated channels (ionotrophic) and metabotropic

receptors.

11 Three ionotrophic receptor types have been identified, based on their

affinity for selective agonists. These include N-methyl-D-aspartate (NMDA),

alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA), and

kainate

receptors. Neurons frequently contain more than one of these receptors types

on the synaptic membranes.

The ionotrophic receptors control the passage of sodium, potassium, and

calcium

through membrane channels, which in turn initiates neuronal depolarization

(excitation). Most important to the excitotoxic process is calcium

accumulation

within the cytosol following glutamate receptor activation. Intracellular

calcium

triggers numerous cellular reactions including the activation of nitric

oxide synthase

and protein kinase C.12 These in turn can activate free radical generation

and lipid peroxidation as well as eicosanoid activation, should glutamate

persist

too long in its receptor.13 These processes play a major role in excitotoxic

injury

and neuronal death.

Three types of metabotropic receptors and eight subtypes of these receptors

have been identified through cloning techniques. They operate mainly by GTP

(guanine triphosphate) binding proteins or G-proteins. 14 When these

receptors

are stimulated by glutamate, the G-protein within the cell membrane is

activated,

which in turn activates several second messengers within the neuron,

including

IP3 (inositol 1,4,5-trisphosphate), cAMP (cyclic adenine monophosphate), or

cGMP (cyclic guanine monophosphate). There is also evidence that they

regulate

intracellular calcium.16 Two of the metabotropic receptors are thought to be

neuroprotective

and one is capable of triggering excitotoxicity.

Free radicals and lipid peroxidation products generated by excitotoxicity

have

been shown to damage dendrites and synaptic connections, and, if unrelieved,

lead to neuronal destruction.16 Likewise, free radicals caused by other

processes

have been shown to trigger excitotoxicity by impairing glutamate removal and

by

activating microglia, which contain abundant stores of glutamate.17

Excitoxicity: a possible central mechanism in fluoride neurotoxicity 305

Fluoride 2004;37(4)

It has also been shown that one of the lipid peroxidation products,

4-hydroxynonenal

(4-HNE), specifically impairs synaptic function and inhibits glutamate

removal by the glutamate transport proteins.18 This lipid peroxidation

product,

though less abundant than malondialdehyde, is significantly more neurotoxic.

Any process that precipitates lipid peroxidation also precipitates the

production

of 4-HNE. Therefore, even if fluoride does not directly trigger

excitotoxicity, it

will do so indirectly by impairing glutamate removal and by generating

reactive

oxygen intermediates and lipid peroxidation products.

A study from China found that sodium fluoride significantly increased nitric

oxide synthase (NOS) activity.19 Interestingly, excitotoxins also stimulated

NOS

activity, which increases intracellular nitric oxide (NO) content. This is

of particular

importance because NO combines readily with superoxide forming the very

powerfully toxic peroxynitrite radical, which plays a major role in all

neurodegenerative

diseases, primarily by damaging mitochondrial energy production,

inhibiting glutamate re-uptake, and stimulating lipid peroxidation.20- 21

Fluoride

has also been shown to inhibit superoxide dismutase, which would increase

intracellular

levels of the superoxide radical, the substrate for peroxynitrite formation.

22

Another related neurotoxin, aluminum, is known to produce a dramatic

increase

in brain free radical generation and lipid peroxidation both directly and by

increasing neuronal and glial iron levels.23 In addition, melanin has a high

affinity

for aluminum, making neuromelanin-containing neurons in the substantia

nigra pars compacta significantly more vulnerable to free radical and lipid

peroxidation

injury.24 Aluminum accumulation and focal increases in reactive oxygen

species and lipid peroxidation in this nucleus have been demonstrated in

Parkinson's disease.25

Another mechanism by which fluoride might increase brain free radical

generation

and lipid peroxidation would be through activation of protein kinase C by a

fluoroaluminum complex. It is known that a major mechanism by which

glutamate induces excitotoxicity is activation of protein kinase C. Blocking

this

enzyme affords significant protection against excitotoxicity. Lead

dramatically

increases protein kinase C activity in a manner similar to glutamate,

thereby triggering

excitotoxicity.26 Fluoride, in the form of silicofluorides in drinking water

has been found to increase blood lead levels significantly, indicating an

indirect

connection between fluoride, free radical generation, and excitotoxicity.27

Because of the intimate connection between excitotoxicity, free radical

generation,

and lipid peroxidation, one can safely assume that fluoride can at least

initiate

the process indirectly and because of chronic exposure seen with water

fluoridation, one would expect an eventual increase in

neurodegeneration-associate

disorders such as Alzheimer's dementia, ALS, and Parkinson's disease.

2. Inhibition of antioxidant enzymes

Closely connected with excitotoxicity-precipitated free radical generation

and

lipid peroxidation is the eventual depletion of antioxidant defenses.

Several stud306

Blaylock

Fluoride 2004;37(4)

ies have demonstrated that fluoride toxicity, as well as excitotoxic injury,

is associated

with selective antioxidant depletion.28-30

Fluoride has been shown to inhibit certain antioxidant enzymes and

molecules,

such as superoxide dismutase (SOD), glutathione reductase, glutathione

peroxidase,

catalase, and glutathione.31 This would not only increase free radical

injury

but would also enhance excitotoxicity, since reactive oxygen species as well

as

nitrogen species and lipid peroxidation products can trigger the excitotoxic

process.

32 Antioxidant enzyme inhibition would necessarily enhance the toxicity of

other neurotoxic elements, pesticides, herbicides, and environmental

pollutants.

Another mechanism for magnifying the harmful effects of both fluoride and

excitotoxins on the brain would be inhibition of melatonin. Melatonin, a

hormone

produced by the pineal gland, has been shown to have powerful neutralizing

effects on free radicals and lipid peroxidation and to increase the levels

of several

of the antioxidant enzymes in the brain including SOD, glutathione

reductase,

glutathione peroxidase, catalase, and glutathione itself.33

A recent study has shown that fluoride significantly inhibits the release of

melatonin from the pineal gland and that fluoride accumulates in the gland

in

very large concentrations in individuals drinking fluoridated water.34

Ironically,

glutamate and aspartate also powerfully inhibit melatonin release from the

pineal

gland and do so by a metabotropic receptor.35 Conceivably, fluoride inhibits

release of pineal melatonin by elevating glutamate levels. Since no research

has

been reported looking for this connection we do not know.

A recent study revealed that babies with the lowest melatonin production had

the most neurobehavioral problems.36 Melatonin levels are also lower in the

cerebrospinal

fluid (CSF) of Alzheimer's patients as compared with normal individuals.

37 The fact that fluoride lowers melatonin production would indicate that

risk

of neurodegeneration in both instances would be elevated.38

3. Inhibition of mitochondrial energy enzymes

Another connection between glutamate excitotoxicity and fluoride toxicity is

related to inhibition of brain energy production. Several studies have shown

that

anything which suppresses neuronal energy production, especially

mitochondrial

energy production, greatly enhances excitotoxic sensitivity.39-41 In fact,

when

neuronal energy production is low, even physiological levels of excitotoxins

such

as glutamate can trigger excitotoxicity.

Fluoride is also known to inhibit cellular energy producing enzymes,

including

mitochondrial electron transport enzymes. It does this both directly, as in

the case

of glycolytic and Kreb's cycle enzymes,42 and indirectly, as in the case of

the

mitochondrial enzymes by the effect of peroxynitrite.43 Vani and Reddy

demonstrated

suppression of both antioxidant enzymes and energy generating enzymes

in female mice treated with 20 mg of fluoride/kg bw for 14 days.22

The importance of neuronal energy suppression by fluoride lies in the fact

that

that mitochondrial energy suppression is intimately connected as an early

event

to neurodegenerative diseases such as Alzheimer's dementia and Parkinson's

disExcitoxicity:

a possible central mechanism in fluoride neurotoxicity 307

Fluoride 2004;37(4)

ease.44-46 Since fluoride can inhibit these enzymes, even in low

concentrations,

there is an increased likelihood that excitotoxicity plays a significant

role in this

process. Likewise, it should be appreciated that Mullenix et al have shown

that

fluoride accumulates in various brain areas of the rat, particularly the

hippocampus,

resulting in higher fluoride levels in the brain than are seen in the

blood.47

The hippocampus is one of the most sensitive areas of the brain to a

multitude of

neurotoxic events.

4. Inhibition of glutamate transporters

One of the most important ways glutamate concentrations are controlled in

the

nervous system is by a series of glutamate transport proteins. Thus far,

five such

transporters have been demonstrated by cloning techniques.48 Of particular

importance are GLAST (cloned glutamate/aspartate transporter) and GLT-1

(glutamate transporter-1). These transporters are associated with either the

glial

cells or the neurons themselves. The glial transporters (GLAST and GLT-1)

bind

to synaptically released glutamate and transport it to the interior of the

glial cells.

The neuronal transporters bind the glutamate and transfer it to the interior

of the

presynaptic terminal.

Considerable evidence points to impairment of these transporters as major

players

in neurodevelopmental disorders and neurodegenerative diseases.49 The

function

of these transporters is altered by a number of commonly encountered toxins

including mercury,50 aluminum,51 iron,52 cytokines,53 eicosanoids (PGE2),54

and 4-HNE.55 In fact, mercury has been shown to inhibit the glutamate

transporters

at concentrations below those that are cytotoxic.56 Anything that increases

free radical generation and lipid peroxidation impairs glutamate transport.

Aluminum inhibition of glutamate transporters is of special interest because

of

the frequent and ready interaction of aluminum and fluoride to form a

biologically

reactive complex. Although no one has apparently examined the occurrence

of fluoride-aluminum complexes as the common inhibitor involved, the

possibility

is quite high. This is because of the chemical avidity of fluoride for

aluminum

and the fact they frequently occur together in nature.

Even without the direct involvement of a fluoroaluminum complex, the fact

that fluoride is known to cause a seven-fold increase in the absorption of

aluminum

past gut barriers is of significant concern.57 In addition, fluoride

enhances

the passage across the blood-brain barrier. In several studies, fluoride

added to

drinking water doubled brain aluminum levels, thus increasing the likelihood

of

glutamate transporter inhibition.58,59

Aluminum glutamate, which is formed in the GI tract, has been shown to alter

the blood-brain barrier making it more permeable to normally excluded

toxins.60

In addition, it enhanced both aluminum and glutamate concentrations in the

brain, significantly increasing the risk of excitotoxicity.

308 Blaylock

Fluoride 2004;37(4)

THE ALUMINUM-FLUORIDE CONNECTION

As mentioned in the introduction, aluminum interacts with fluoride to form a

fluoroaluminum complex that mimics phosphate groups in biological systems.61

By this mechanism, it could also activate the G-proteins in cell membranes.

As

we have seen, the metabotropic receptors are activated by a G-protein

mechanism.

In addition, numerous cells in the body utilize the G-protein second

messenger

receptor system, including endothelial cells, lymphocytes, osteoblasts,

other neurotransmitters (dopamine, norepinephrine, acetylcholine, serotonin,

neuropeptides, and opioids), and glucagon.

Activation of metabotropic excitatory receptors by an aluminum-fluoride

complex

could initiate excitotoxicity as shown by Lan and coworkers.62 Because the

aluminum-fluoride complex accumulates in the brain, it would also be

expected

to cause prolonged neurotoxicity, leading eventually to neurodegeneration

and

synaptic loss.

The aluminum-fluoride complex has been shown to produce neuronal loss in

the CA1 and CA-4 areas of the hippocampus when given to animals as 0.5 ppm

in drinking water.59 The toxic effect may be related to a combination of

effects,

including impairment of energy-producing enzymes, impaired dephosphorylation

of hyperphosphorylated tau-protein, increased neuronal iron concentration,

elevated

free radical and lipid peroxidation levels, and impaired DNA repair, all of

which are related to excitotoxicity.

Another toxic effect of aluminum, and possibly a fluoroaluminum complex, is

the activation of microglia. These are resident immune cells within the

nervous

system, which are normally quiescent, but are easily activated by a number

of

environmental and biological agents, such as viruses, mycoplasma, bacteria,

aluminum,

mercury, and several pesticides.63

Once activated, microglia generate and secrete a number of neurotoxic

compounds,

including two powerful excitotoxins: glutamate and quinolinic acid.64

The combination of excitotoxin secretion and cytokine production greatly

increases the concentration of free radicals and lipid peroxidation products

in the

brain. No one has looked at the possibility of fluoride-induced microglial

activation.

Yet, one would expect the fluoroaluminum complex to activate microglia,

since aluminum alone is a powerful activator.65

Chronic microglial activation has been associated with a number of

neurodegenerative

processes, including strokes, multiple sclerosis, brain trauma, experimental

allergic encephalomyelitis (EAE), Alzheimer's dementia, Parkinson's

disease, and ALS.3 Because both aluminum and fluoride accumulate in the

brain

and have their highest concentrations in the hippocampus and neocortex, one

would expect chronic microglial activation as well. At least one study noted

reactive

gliosis (microglial activation) in association with fluoride brain

toxicity.66

Excitoxicity: a possible central mechanism in fluoride neurotoxicity 309

Fluoride 2004;37(4)

FLUORIDE: A SPECIAL DANGER TO THE DEVELOPING BRAIN

The brain undergoes one of the fastest growth and development rates of any

portion of the human body during embryogenesis. This occurs especially

during

the last trimester and first two years of life, a period called the brain

growth spurt.

This involves not only the rapid development of synaptic connections

(synaptogenesis)

and pathway development, but also refinement of all of the synaptic

connection

made during this period. One way glutamate does this is by stimulating

the growth cones that guide neural pathways to their intended destination.

The

brain develops far greater synaptic connections than are needed during this

" brain

growth spurt " and as a result, synaptic connections are removed in a process

referred to as pruning.

Connected to this pruning process, as well as to synaptogenesis and pathway

development, is the level of glutamate within the brain. The rise and fall

of brain

glutamate levels during development controls these processes, and is finely

tuned

throughout brain development.67 Too much glutamate overprunes the synapses

and dendrites, whereas too little results in an excess of un-needed

connections.68

Both can result in severe neurodevelopmental problems.

Recent studies have revealed that the glutamate transport proteins also play

a

significant role in the development of the brain.69,70 As shown by these

studies,

anything that alters transporter function can affect brain development. By

interfering

with neuronal energy production, neurotransmitter levels (especially

glutamate), free radical generation and growth cone function, fluoride can

have

significant harmful effects on neurodevelopment.

In addition, fluoride has also been found to inhibit thyroid function and

thereby

alter early neuron migration in the developing fetus.71 This can result in

irreversible

changes in the fetal brain.

A CALL FOR FURTHER RESEARCH

It is obvious from this short review that more research needs to be done in

this

area. We need data on both the effects of fluoride and fluoroaluminum on the

glutamate transporter proteins and on the exact mechanism of free radical

generation

being caused by fluoride. In addition, we need studies to see if fluoride

can

cause chronic microglial activation and neurodegeneration.

Because of the growing number of studies showing a strong connection

between aluminum accumulation in the brain and neurodegenerative diseases,

studies need to be done to see if the aluminum in neurofibrillary tangles

and

senile plaques is in fact fluoroaluminum. Further studies are also needed to

see if

fluoroaluminum passes along olfactory axons into the entorhinal area as has

been

demonstrated for aluminum itself.72 This would not only provide direct

access to

the area of the brain showing the earliest changes of Alzheimer's dementia,

but

would allow lower concentrations in the drinking water to produce higher

concentrations

in the hippocampal area than would be attainable from blood.

310 Blaylock

Fluoride 2004;37(4)

In addition, special studies are needed using silicofluorides to see if

their toxicity

to the nervous system differs from that of sodium fluoride. Along this same

line, we need data on the possibility of additive and even synergic

toxicities when

fluoride is combined with mercury, lead, cadmium, and other known

neurotoxins.

Although progress has been made on nutrient-based neuroprotection against

fluoride toxicity, more research needs to be pursued.73-77 Chinoy and Sharma

found that both vitamin E and D3 reversed the toxic effect of fluoride on

male

reproductive organs and that a combination of the two antioxidants

completely

reversed the toxicity.78 In a recent study, Chinoy and Shah found that a

combination

of vitamin C and E and calcium could reverse the toxic effects of both

fluoride

and arsenic on multiple biochemical parameters, including suppression of

dehydroascorbic acid, glutathione, glutathione peroxidase, and SOD in the

brains

of mice.79 If excitotoxicity indeed plays a significant role in fluoride

toxicity, we

need to apply some of the methods used to protect against excitotoxicity,

such as

increasing the intake of methylcobalamin, melatonin, selenium, the B

vitamins,

vitamins C, E, D, and K, along with metabolic stimulants such as pyruvate,

malate, CoQ10, acetyl-L-carnitine, R-lipoic acid, and ginkgo biloba. Of

special

importance is supplementation with magnesium, which has been shown to block

the NMDA glutamate receptor and decrease free radical production.

One area of particular interest is the use of flavonoids as

neuroprotectants. Plant

flavonoids are known to be the most versatile and powerful antioxidants

known,

and one of the few antioxidants that will neutralize peroxynitrite.80 In

addition,

they can chelate metals, reduce inflammation, block eicosanoid production,

and

inhibit enzymes such as protein kinase C, which is critical to

excitotoxicity and

lead neurotoxicity.81 A recent study by Juzyszyn and co-workers found that

quercetin

sulfonate, a water-soluble form of the flavonoid quercetin, protected liver

and kidney cells from ammonium fluoride suppression of mitochondrial energy

production.82

Finally, we need more data on the concentration and accumulation of fluoride

in other calcified areas of the brain beside the pineal gland. For example,

calcification

of the basal ganglion is seen in a small number of individuals. In the past,

this was considered an asymptomatic condition occurring in 0.3% of the

population

examined.83 While basal ganglion calcification has been noted in a number

of disorders, of particular interest is its appearance in Down's syndrome.

One

study on autopsied Down's brains found calcification in 45% in the area of

the

basal ganglion and increased calcification there with increasing age.84

Newer

studies have shown that a significant number of these individuals have

symptoms

related to basal ganglion dysfunction as well as neuropsychiatric

disturbances.85

In addition, recent studies has shown that excitotoxicity induces

calcification

deposits in the brain, which also contain aluminosilicates.86 Should these

calcifications

accumulate fluoride in high concentrations as found in pineal

calcifications,

one would expect damage to adjacent neurons and glia. With widespread

fluoridation of drinking water, one would also expect higher fluoride

concentrations

in these calcified structures than in the past.

Excitoxicity: a possible central mechanism in fluoride neurotoxicity 311

Fluoride 2004;37(4)

It is obvious from this review that there is an intimate connection between

the

neurotoxicity of fluoride, aluminum, and glutamate that needs further

attention. It

is also obvious that excitotoxicity plays some role in this process, perhaps

a central

one.

REFERENCES

1 Lipton SA, Rosenberg PA. Excitatory amino acids as a final common pathway

for neurological disorders.

N Eng J Med 1994;330:613-22.

2 Blaylock RL. The central role of excitotoxicity in autism spectrum

disorders. Journal of the American

Nutraceutical Association (JANA) 2003;6:7-19.

3 Blaylock RL. Interaction of cytokines, excitotoxins and reactive nitrogen

and oxygen species in

autism spectrum disorders. Journal of the American Nutraceutical Association

(JANA) 2003;6:21-

35.

4 Blaylock RL Chronic microglial activation and excitotoxicity secondary to

excessive immune stimulation:

Possible factors in Gulf War Syndrome and autism. Journal of American

Physicians and

Surgeons 2004;9:46-51.

5 Szatkowski M, Attwell D. Triggering and execution of neuronal death in

brain ischemia: two

phases of glutamate release by different mechanisms. Trends Neurosci

1994;17:359-65.

6 Jensen AA, Brauner-Osborne H. Pharmacological characterization of human

excitatory amino acid

transporters EAAT1, EAAT2 and EAAT3 in a fluorescence-based membrane

potential assay. Biochem

Pharmacol 2004;67:2115-27.

7 Lucas DR, Newhouse JP. The toxic effect of sodium L-glutamate on the inner

layers of the retina.

AMA Arch Ophthalmol 1957;58:193-201.

8 Olney JW. Brain lesions, obesity and other disturbances in mice treated

with monosodium

glutamate. Sci 1969; 164:719-21.

9 Hinoi E, Takarada T, Ueshima T, Tsuchihashi Y, Yoneda Y. Glutamate

signaling in peripheral tissues.

Eur J Biochem. 2004;271:1-13.

10 Trudeau LE. Glutamate co-transmission as an emerging concept in monoamine

neuron function. J

Psychiatry Neurosci. 2004;29:296-310.

11 Simeone TA, RM, Rho JM. Molecular biology and ontogeny of

glutamate receptors in the

mammalian central nervous system. J. Child Neurol 2004;19:343-60.

12 Lan JY, Skeberdis VA, Jover T, Grooms SY, Lin Y, Araneda RC, et al.

Protein kinase C modulates

NMDA receptor trafficking and gating. Nat Neurosci 2001;4:382-90.

13 Babu GN, Bawari M, Ali MM. Lipid peroxidation potential and antioxidant

status of circumventricular

organs of rat brain following neonatal monosodium glutamate. Neurotoxicology

1994;15:773-7.

14 Minoshima T, Nakanishi S. Structural organization of the mouse

metabotropic glutamate receptor

subtype 3 gene and its regulation by growth factors in cultured cortical

astrocytes. J Biochem

(Tokyo) 1999;126:889-96.

15 Baskys A. Metabotropic receptors and 'slow' excitatory actions of

glutamate agonists in the hippocampus.

Trends Neurosci 1992;15:92-6.

16 Isokawa M, Levesque MF. Increased NMDA responses and dendritic

degeneration in human epileptic

hippocampal neurons in slices. Neurosci Lett 1991;132:212-6.

17 Pellegrini-Giampietro DE, Cherici G, Alesiani M, Carla V, Moroni F.

Excitatory amino acid release

from rat hippocampal slices as a consequence of free-radical formation. J

Neurochem

1988;51:1960-3.

18 Blanc EM, Keller JN, Fernandez S, Mattson MP. 4-Hydroxynonenal, a lipid

peroxidation product,

impairs glutamate transport in cortical astrocytes. Glia 1998;22:149-60.

19 Xu S, Shu B, Chen Z. Effect of fluoride on activities of nitric oxide

synthase in rat brain [abstract].

Fluoride 2001;34:84.

20 Cassina R, Radi R. Differential inhibitory action of nitric oxide and

peroxynitrite on mitochondrial

electron transport. Arch Biochem Biophys 1996;328:309-16.

312 Blaylock

Fluoride 2004;37(4)

21 Bolanos JP, Almeida A, V, Peuchen S, Land JM, JB. Nitric

oxide-mediated mitochondrial

damage in the brain: mechanisms and implications for neurodegenerative

diseases. J

Neurochem 1997:68:2227-40.

22 Vani LM, Reddy KP. Effects of fluoride accumulation on some enzymes of

brain and gastrocnemius

muscle of mice. Fluoride 2000; 33:17-26.

23 Mundy WR, Freudenrich TM, Kodavanti PR. Aluminum potentiates

glutamate-induced calcium

accumulation and iron-induced oxygen free radical formation in primary

neuronal cultures. Mol

Chem Neuropathol 1997;32:41-57.

24 Meglio L, Oteiza PI. Aluminum enhances melanin-induced lipid

peroxidation. Neurochem Res

1999;24:1001-8.

25 Good PF, Olanow CW, Perl DP. Neuromelanin-containing neurons of the

substantia nigra accumulate

iron and aluminum in Parkinson's disease: A LAMMA study. Brain Res 1992;593:

343-6.

26 Naarala JT, Loikkanen JJ, Ruotsalainen MH, Savilainen KM. Lead amplifies

glutamate-induced

oxidative stress. Free Radic Biol Med 1995;19:689-93.

27 Coplan MJ, Masters RD. Silicofluorides and fluoridation. Fluoride

2001;34: 161-4.

28 Shivarajashankara YM, Shivashankara AR, Bhat GP, Rao SH, Brain lipid

peroxidation and antioxidant

systems of young rats in chronic fluoride intoxication. Fluoride

2002;35:197-203.

29 Inkielewicz I, Krechniak J Fluoride effects on glutathione peroxidase and

lipid peroxidation in rats.

Fluoride 2004;37:7-12.

30 Singh K, Ahluwalia P. Studies on the effect of monosodium glutamate [MSG]

administration on

some antioxidant enzymes in the arterial tissue of adult male mice. J Nutr

Sci Vitaminol (Tokyo)

2003; 49:145-8.

31 Li J, Cao S. Recent studies on endemic fluorosis in China [editorial].

Fluoride 1994; 27:125-8.

32 Siesjo BK, Bengtsson F. Calcium fluxes, calcium antagonists, and

calcium-related pathology in

brain ischemia, hypoglycemia, and spreading depression: a unifying

hypothesis. J Cereb Blood

Flow Metab 1989;9:127-40.

33 Reiter RJ, Tan DX, Osuna C, Gitto E. Actions of melatonin in the

reduction of oxidative stress: a

review. J Biomed Sci 2000;7:444-58.

34 Luke J. Fluoride deposition in the aged human pineal gland. Caries Res

2001;35: 125-8.

35 Yamada H, Yatsushiro S, Ishio S, Hayashi M, Nishi T, Yamamoto A.

Metabotropic glutamate

receptors negatively regulate melatonin synthesis in rat pinealocytes. J

Neurosci 1998; 18:2056-62.

36 Tauman R, Zisapel N, Laudon M, Nehama H, Sivan Y. Melatonin production in

infants. Pediatr

Neurol 2002;26:379-82.

37 Lima AC, Louzada PR, De Mello FG, Ferreira ST. Neuroprotection against

Abeta and glutamate

toxicity by melatonin: are GABA receptors involved? Neurotox Res

2003;5:323-7.

38 Gao HX, Zhang LX. Anatagonistic effects of melatonin on glutamate-induced

neurotoxicity in rat

hippocampal neurons. Sheng Li Xue Bao 1999;51:430-4.

39 Nicholls DG, Budd SL. Mitochondria and neuronal glutamate excitotoxicity.

Biochim Biophys

Acta 1998;1366:97-112.

40 Beal MF, Hyman BT, Koroshetz W. Do defects in mitochondrial energy

metabolism underlie the

pathology of neurodegenerative diseases? Trends Neurosci 1993;16:125-31.

41 Henneberry RC. The role of neuronal energy in neurotoxicity of excitatory

amino acids. Neurobiol

Aging 1989;10:611-3.

42 Dousset JC, Rioufol C, Philibert C, Bourbon P. Effects of inhaled HF on

cholesterol, carbohydrate

and trioxycarboxylic acid metabolism in guinea pigs. Fluoride

1987;20:137-41.

43 Ebadi M, Sharma SK. Peroxynitrite and mitochondrial dysfunction in the

pathogenesis of Parkinson's

disease. Antioxid Redox Signal 2003; 5:319-35.

44 Meltzer CC, Zubieta JK, Brandt J, Tune LE, Mayberg HS, Frost JJ. Regional

hypometabolism in

Alzheimer's disease as measured by positron emission tomography after

correction for effects of

partial volume averaging. Neurology 1996;47:454-61.

45 Schapira AH, Gu M, Taanman JW, Tabrizi SJ, Seaton T, Cleeter M, et al.

Mitochondria in the etiology

and pathogenesis of Parkinson's disease. Ann Neurol 1998;44 Suppl 1:S89-S98.

Excitoxicity: a possible central mechanism in fluoride neurotoxicity 313

Fluoride 2004;37(4)

46 Gibson GE, Park LC, Zhang H, Sorbi S, Calingasan NY. Oxidative stress and

a key metabolic

enzyme in Alzheimer brains, cultured cells, and an animal model of chronic

oxidative deficits. Ann

NY Acad Sci 1999;893:79-94.

47 Mullenix PJ, Denbesten PK, Schunior A, Kernan WJ. Neurotoxicology of

sodium fluoride in rats.

Neurotoxicol Teratol 1995;17: 169-77.

48 Seal RP, Amara SG. Excitatory amino acid transporters: a family in flux.

Annu Rev Pharmacol

Toxicol 1999; 39:431-56.

49 Maragakis NJ, Rothstein JD. Glutamate transporters: animal models to

neurologic disease. Neurobiol

Dis 2004; 15:461-73.

50 s N. Specificity and reversibility of the inhibition by HgCl2 of

glutamate transport in astrocyte

cultures. J Neurochem 1988; 50:1117-22.

51 Sass JB, Ang LC, Juurlink BH. Aluminum pretreatment impairs the ability

of astrocytes to protect

neurons from glutamate mediated toxicity. Brain Res 1993;621:207-14.

52 Ueda Y, Willmore LJ. Sequential changes in glutamate transporter protein

levels during Fe3+-

induced epileptogenesis. Epilepsy Res 2000; 39:201-9.

53 Hu S, Sheng WS, Ehrlich LC, PK, Chao CC. Cytokine effects on

glutamate uptake by

human astrocytes. Neuroimmunomodulation 2000;7:153-9.

54 Lundy DF, McBean GJ. Pre-incubation of synaptosomes with arachidonic acid

potentiates inhibition

of [3H] D-aspartate transport. Eur J Pharmacol 1995;291:273-9.

55 Keller JN, Mark RJ, Bruce AJ, Blanc E, Rothstein JD, Uchida K et al.

4-Hydroxynonenal, an aldehydic

product of membrane lipid peroxidation, impairs glutamate transport and

mitochondrial function

in synaptosomes. Neuroscience 1997;80:685-96.

56 Aschner M, Du YL,Gannon M, Kimelberg HK. Methylmercury-induced

alterations in excitatory

amino acid transport in rat primary astrocyte cultures. Brain Res

1993;602:181-6.

57 Allain P, Gauchard F, Krari N. Enhancement of aluminum digestive

absorption by fluoride in rats.

Res Commun Mol Pathol Pharmacol 1996;91:225-31.

58 Varner JA, Horvath WJ, Huie CW, Naslund HR, Isaacson RL. Chronic aluminum

fluoride administration.

I. Behavioral observations. Behav Neural Biol 1994;61:233-41.

59 Varner JA, Jenson KF, Horvath W, Isaacson RL. Chronic administration of

aluminum-fluoride or

sodium-fluoride to rats in drinking water: alterations in neuronal and

cerebrovascular integrity.

Brain Res 1998;784:284-98.

60 Deloncle R, Guillard O, Huguet F, Clanet F. Modification of the

blood-brain barrier through

chronic intoxication by aluminum glutamate. Possible role in the etiology of

Alzheimer's disease.

Biol Trace Elem Res 1995;47:227-33.

61 Strunecka A, Strunecky O, Patocka J. Fluoride plus aluminum: useful tools

in laboratory investigations,

but messengers of false information. Physiol Res 2002;51:557-64.

62 Lan JY, Skeberdis VA, Jover T, Zheng X, MV, Zukin RS. Activation

of metabotropic

glutamate receptor 1 accelerates NMDA receptor trafficking. J Neurosci

2001;21:6058-68.

63 Thoulmond S, Parnet P, Linthorst AC. When cytokines get on your nerves:

cytokine networks and

CNS pathologies. Trends Neurosci 1996;19:409-10.

64 Tavares RG, Tasca CL, Santos CE, Alves LB, Porciuncula LO, Emanuelli T,

et al. Quinolinic acid

stimulates synaptosomal glutamate release and inhibits glutamate uptake into

astrocytes. Neurochem

Int 2002;40:621-7.

65 Tsunoda M, Sharma RP. Modulation of tumor necrosis factor alpha

expression in mouse brain after

exposure to aluminum in drinking water. Arch Toxicol 1999;73:419-26.

66 Shivarajashankara YM, Shivashankara AR, Bhat PG, Roa SM, Roa SH.

Histological changes in the

brain of young fluoride-intoxicated rats. Fluoride 2002;35:12-21.

67 Komuro H, Rakic P. Modulation of neuronal migration by NMDA receptors.

Science 1993;260:95-

7.

68 Marret S, Gressens P, Evarard P. Arrest of neuronal migration by

excitatory amino acids in hamster

developing brain. Proc Natl Acad Sci USA 1996;93:15463-8.

69 Bar-Peled O, Ben-Hur H, Biegon A, Groner Y, Dewhurst S, Furuta A.

Distribution of glutamate

transporter subtypes during brain development. J Neurochem 1997;69:2571-80.

314 Blaylock

Fluoride 2004;37(4)

70 Shibata T, Watanabe M, Tanaka K, Wada K, Inoue Y. Dynamic changes in

expression of glutamate

transporter mRNAs in developing brain. Neuroreport 1996;7:705-9.

71 Trabelsi M, Guermazi F, Zeghal N. Effect of fluoride on thyroid function

and cerebellar development

in mice. Fluoride 2001;34:165-73.

72 Perl DP, Good PF. Uptake of aluminum into central nervous system along

nasal-olfactory pathways.

Lancet 1987;1:1028.

73 Susheela AK, Bhatnagar M. Reversal of fluoride induced cell injury

through elimination of fluoride

and consumption of diet rich in essential nutrients and antioxidants. Mol

Cell Biochem 2002;234-

235:335-40.

74 Guna Sherlin DM, Verma RJ. Vitamin D ameliorates fluoride-induced

embryotoxicity in pregnant

rats. Neurotoxicol Teratol 2001;23:197-201.

75 Verma RJ, Sherlin DM. Vitamin C ameliorates fluoride-induced

embryotoxicity in pregnant rats.

Hum Exp Toxicol 2001:619-23. [abstract in Fluoride 2002;35:131].

76 Chinoy NJ, Sequeira E, Narayana MV. Effects of vitamin C and calcium on

the reversibility of fluoride-

induced alterations in spermatozoa of rabbits. Fluoride 1991;24:29-39.

77 Gupta SK, Gupta RC, Seth AK, Gupta A. Reversal of fluorosis in children.

Acta Paediatr Jpn

1996;38:513-9.

78 Chinoy NJ, Sharma A. Amelioration of fluoride toxicity by vitamins E and

D in reproductive functions

of male mice. Fluoride 1998;31:203-16.

79 Chinoy NJ, Shah SD. Biochemical effects of sodium fluoride and arsenic

trioxide toxicity and their

reversal in the brain of mice. Fluoride 2004;37(2):80-7.

80 Blaylock RL. Neurodegeneration and aging of the central nervous system:

prevention and treatment

by phytochemicals and metabolic nutrients. Integrative Med 1998;1:117-33.

81 Blaylock RL. New developments in the prevention and treatment of

neurodegenerative diseases

using nutraceuticals and metabolic stimulants. Journal of the American

Nutraceutical Association

(JANA) 2002;5:15-32.

82 Juzyszyn Z, Czerny B, Myoeliwiec Z, Put A, Enhancement of kidney and

liver respiratory activity

by quercetin sulfonates in rats chronically exposed to ammonium fluoride.

Fluoride 2002;35: 161-

7.

83 Marasco JA Jr, Feczko WA. Basal ganglia calcification in Down's syndrome.

Comput Tomogr

1979;3:111-3.

84 Takashima S, Becker LE. Basal ganglia calcification in Down's syndrome. J

Neurol Neurosurg

Psychiatry 1985;48:61-4.

85 Chiu HF, Lam LC, Shum PP, Li KW. Idiopathic calcification of the basal

ganglia. Postgrad Med J

1993;69:68-70.

86 May N, Prats A, Riveros A, Andres N, Bernal F. Basal ganglia

calcification induced by excitotoxicity:

an experimental model characterized by electron microscopy and X-ray

microanalysis. Acta

Neuropathol (Berl) 1999;98:217-25.

Published by the International Society for Fluoride Research

http://homepages.ihug.co.nz/~spittle/fluoride-journal.htm

Editorial Office: 727 Brighton Road, Ocean View, Dunedin 9051, New Zealand

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i refuse to use flouride in our toothpaste. i have read it is

extremely bad for you on mercola.com i believe and also in natural

cures they don't want you to know. i use spry toothpaste with

xylitol. xylitol is a natural antibacterial and helps to promote

healthy teeth. you can google xylitol to get info on it, there are

many good things about it. you can also add some to thier juices

and bake with it.

jenny

> Hi everyone:

>

> My ASD son uses non fluoride toothpaste. I just

> visited a pediatric dentist for his first check up and

> he was really concerned that my son doesn't get any

> fluoride. I explained to him about trying to reduce

> his toxic load based on his metals test and that he

> gets no chemicals or artificial anything.

>

> He did understand this and knows some of patients who

> are chelating. (he's a special needs dentist)

> However, he said of all the patients he

> knows...fluoride was never a problem.

>

> He said that for my sons permanent teeth he needs the

> fluoride to keep the enamel strong and to of course,

> keep the teeth from decaying.

>

> Any thoughts on the importance of fluoride for our

> kids? Isn't there any " natural " way to prevent

> cavities and make teeth strong at the same time?

>

> thanks. Amy

>

>

>

> ____________________________________________________

> Start your day with - make it your home page

> http://www./r/hs

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Share on other sites

My daughter,too goes to a pediatric/special needs dentist and he

agreed that fluoride wasn't needed. In fact, he went so far as to say

he wouldn't even push toothpaste-just brushing (we use the toddler

fluoride free paste.) He offered to give my daughter flavor-free

toothpaste and to not use flavoring in the glue stuff she needed to

attach something in her mouth...we tasted the NASTY stuff though and

told him to go ahead and add some flavor. ICK! :)

---

In , Amy Allnutt <aallnutt2004@y...>

wrote:

> Hi everyone:

>

> My ASD son uses non fluoride toothpaste. I just

> visited a pediatric dentist for his first check up and

> he was really concerned that my son doesn't get any

> fluoride. I explained to him about trying to reduce

> his toxic load based on his metals test and that he

> gets no chemicals or artificial anything.

>

> He did understand this and knows some of patients who

> are chelating. (he's a special needs dentist)

> However, he said of all the patients he

> knows...fluoride was never a problem.

>

> He said that for my sons permanent teeth he needs the

> fluoride to keep the enamel strong and to of course,

> keep the teeth from decaying.

>

> Any thoughts on the importance of fluoride for our

> kids? Isn't there any " natural " way to prevent

> cavities and make teeth strong at the same time?

>

> thanks. Amy

>

>

>

> ____________________________________________________

> Start your day with - make it your home page

> http://www./r/hs

Link to comment
Share on other sites

> He did understand this and knows some of patients who

> are chelating. (he's a special needs dentist)

> However, he said of all the patients he

> knows...fluoride was never a problem.

I have read some really nasty regression stories about fluoride.

These sites will have more info and research etc

http://www.slweb.org/

http://www.flouridealert.org/

http://www.nofluoride.com/

Dana

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Hi Amy, , either of you in the UK and can tell me the contact details for

your dentist? My Son's teeth are full of plaque and I think its as a result of

combating a huge bacteria problem he's had (we had a 2week course of oral

vancomycin, and that's when the discolouration set in. PS Flouride - no way

would I let it near my son. Can't remember where I read this but it affects our

kids like Chloride. Perhaps Dana has a view on this . All I know is its bad

bad bad and we won't have it in our house!

Eileen and ASD aged 3

david_j_mead <david_j_mead@...> wrote:

My daughter,too goes to a pediatric/special needs dentist and he

agreed that fluoride wasn't needed. In fact, he went so far as to say

he wouldn't even push toothpaste-just brushing (we use the toddler

fluoride free paste.) He offered to give my daughter flavor-free

toothpaste and to not use flavoring in the glue stuff she needed to

attach something in her mouth...we tasted the NASTY stuff though and

told him to go ahead and add some flavor. ICK! :)

---

In , Amy Allnutt <aallnutt2004@y...>

wrote:

> Hi everyone:

>

> My ASD son uses non fluoride toothpaste. I just

> visited a pediatric dentist for his first check up and

> he was really concerned that my son doesn't get any

> fluoride. I explained to him about trying to reduce

> his toxic load based on his metals test and that he

> gets no chemicals or artificial anything.

>

> He did understand this and knows some of patients who

> are chelating. (he's a special needs dentist)

> However, he said of all the patients he

> knows...fluoride was never a problem.

>

> He said that for my sons permanent teeth he needs the

> fluoride to keep the enamel strong and to of course,

> keep the teeth from decaying.

>

> Any thoughts on the importance of fluoride for our

> kids? Isn't there any " natural " way to prevent

> cavities and make teeth strong at the same time?

>

> thanks. Amy

>

>

>

> ____________________________________________________

> Start your day with - make it your home page

> http://www./r/hs

Link to comment
Share on other sites

If you really want to clean his teeth and avoid a dentist altogether try a Sonic

Care toothbrush. They aren't too expensive and they really do work, even with

just water. I love them because they make my teeth feel like I had been to the

dentist. And yes, flouride is really bad...we don't use it either. JMO!

Eileen McLennan <eileen_mclennan@...> wrote:

Hi Amy, , either of you in the UK and can tell me the contact details for

your dentist? My Son's teeth are full of plaque and I think its as a result of

combating a huge bacteria problem he's had (we had a 2week course of oral

vancomycin, and that's when the discolouration set in. PS Flouride - no way

would I let it near my son. Can't remember where I read this but it affects our

kids like Chloride. Perhaps Dana has a view on this . All I know is its bad

bad bad and we won't have it in our house!

Eileen and ASD aged 3

david_j_mead <david_j_mead@...> wrote:

My daughter,too goes to a pediatric/special needs dentist and he

agreed that fluoride wasn't needed. In fact, he went so far as to say

he wouldn't even push toothpaste-just brushing (we use the toddler

fluoride free paste.) He offered to give my daughter flavor-free

toothpaste and to not use flavoring in the glue stuff she needed to

attach something in her mouth...we tasted the NASTY stuff though and

told him to go ahead and add some flavor. ICK! :)

---

In , Amy Allnutt <aallnutt2004@y...>

wrote:

> Hi everyone:

>

> My ASD son uses non fluoride toothpaste. I just

> visited a pediatric dentist for his first check up and

> he was really concerned that my son doesn't get any

> fluoride. I explained to him about trying to reduce

> his toxic load based on his metals test and that he

> gets no chemicals or artificial anything.

>

> He did understand this and knows some of patients who

> are chelating. (he's a special needs dentist)

> However, he said of all the patients he

> knows...fluoride was never a problem.

>

> He said that for my sons permanent teeth he needs the

> fluoride to keep the enamel strong and to of course,

> keep the teeth from decaying.

>

> Any thoughts on the importance of fluoride for our

> kids? Isn't there any " natural " way to prevent

> cavities and make teeth strong at the same time?

>

> thanks. Amy

>

>

>

> ____________________________________________________

> Start your day with - make it your home page

> http://www./r/hs

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