Fluoride's Effects on Bone- Dr. John Lee M.D.

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Fluoride's Effects on Bone-

 

Dr. John Lee M.D.

JoAnn Guest Apr 10, 2004 17:48 PDT

Fluoride's Effects on Bone- Dr. John Lee

 

http://www.johnleemd.net/breaking_news/fluoridation_02.html

-

Fluoride's Effect on BONE - and some related considerations

T.C. Schmidt – 12 March 2000

 

Foreword. Except for the introductory sentence (from a textbook);

one CDC document; two FDA documents; and the NIOSH RTECS (as referenced

 

in the text per se.) the technical basis for this review has been

LIMITED on purpose ONLY to those citations which are retrievable on-

line from the National Library of Medicine (PubMed MEDLINE and/or

Internet Grateful Med TOXLINE).

 

Introduction

 

Bone tissue has long been recognized as a key accumulation site for

some toxic substances – " bones also serve a detoxicating function,

elements such as lead, radium, fluorine and arsenic being removed

from circulation and deposited into bones and teeth "

 

(The Physiological Basis of Medical Practice, 1961).

 

That is, fluoride accumulates in skeletal tissue, concentrating in the

surface layers of the lacunae and canaliculae -- thus helping to

clarify the pathogenesis of the osseous lesions seen in skeletal

fluorosis (Smith, 1985a).

 

Bone samples from cadavers show that fluoride content

of trabecular bone correlates with that of the drinking water --

with histomorphic bone changes becoming markedly increased when water

fluoride content exceeds 1.5-ppm (Alrnala, et al. 1985).

 

Thus, daily intake of fluoride that is deemed beneficial to developing

teeth, if ingested throughout adult life, may lead to skeletal fluorosis

of

varying degrees, plus certain disorders that are now becoming common

in both the middle-aged and elderly (Smith, 1985b).

 

This was more recently substantiated in a review (Diesendorf, et al.

1997) -- showing " a consistent pattern of evidence " .

 

Osteoporosis in the long bones may provide the earliest radiographic

indicator of fluorosis (Lian and Wu, 1986);

with clinical radiological aspects including calcification and/or

ossification of the attachments of the soft- tissue structures to bone,

 

osteosclerosis, osteopenia, growth lines,

and metaphyseal osteomalactic zones (Wang, et al. 1994).

 

More subtle changes as stained section and microradiograph include

interstitial mineralization defects and mottled eperiosteocytic lacunae

(Boivin, et al. 1989) and CT/MR imaging are very helpful in early

diagnosis (Reddy, et al. 1993).

 

 

 

Lessons-Learned from Therapy

 

 

 

Epidemiology

 

Fluoride is a cumulative toxin, adversely affecting the homeostasis

of bone mineral metabolism.

 

Total ingested fluoride is the most important factor determining the

clinical course of osteo-fluorosis, which is on the increase world-wide

(Krishnamachari, 1986).

 

A level of 4-10 ppm in drinking water causes progressive ankylosis of

various joints and crippling deformities irrespective of other

variables –

as evidenced by skeletal radiology and scintigraphy, cross-correlated

with urinary and serum fluoride levels (Gupta, et al. 1993).

 

At greater than 4-ppm for longer than 10-years (Haimanot, 1990) there is

generalized osteophytosis and sclerosis with reduction in diameter of

nter-vertebral foramina and spinal clonal.

 

Animal studies

(Turner, et al. 1996) showed fluoridated water equivalent to only 3-ppm

in humans results in reduced bone strength after 6-months -- when

accompanied by renal deficiency.

Similarly, comparison of a control community having a fluoride content

of 1-ppm and that of another with a 4-ppm level (Sowers, et al. 1991)

showed a 95% confidence-interval (CI) for the 5-year relative risk (RR)

for women of any fracture of 1.0-4.4 -- and for wrist, spine or hip it

was 1.1-4.7.

 

That such increase in risk correlates with fluoride accumulation was

corroborated based on a study of toenail fluoride concentration in

more than 64,000 women (Feskanich, et al. 1998) -- comparing the

highest quartile against the lowest quartile provided a 95% CI 0.2-

4.0 for hip fracture RR, and 0.8-3.1 for forearm fracture.

 

That detrimental accumulation occurs due to water fluoridation at

the " public health goal " was shown by comparing fluoridated and non-

fluoridated areas (Alhava, et al. 1980) with the highest

accumulations being in women with severe osteoporosis.

 

That reduction in bone strength presents clinically at the " public

health goal " --

the 95% CI RR for hip fracture of fluoridated vs non-fluoridated

(Jacobsen, et al. 1992) was 1.06-1.10 for women and 1.13-1.22 for

men. Similarly, for femoral neck fracture the 95% CI of RR was 1.08-

1.46 for women and 1.00-1.81 for men (Danielson, et al. 1992) -- and

a study (Kurttio, et. al. 1999) showed a 95% CI for hip fracture

among younger women of 1.16-3.76.

 

Related Considerations

 

During treatment with fluoride for spinal osteoporosis, some

patients suffered spontaneous bilateral hip fractures (Gerster, et al.

1983) with histological examination revealing severe osteo-fluorosis --

attributed to excessive retention of fluoride due to renal

insufficiency.

 

Fluoride is nephrotoxic, causing lesions of kidney tubule (Kassabi, et

al. 1981).

 

Acute renal failure results from accidental industrial exposure to

fluoride (Usada, et al. 1998); with the nephrotoxic effects related to

serum fluoride level.

 

Not only does this result in aluminum deposition into bone (Ittel, et

al. 1992); as fluoride elimination is via the kidney (Kono, 1994) and

decreased kidney function results in increasing serum fluoride, a

vicious cycle is not unlikely (Marumo and Li; 1996).

 

Elevated PTH is not uncommon in fluorosis (Srivastava, et al. 1989) and

is a uremic toxin playing a major role in nervous system dysfunction

(Smogorzewski and Massry, 1995) and development of hypertension

(Uchimoto, et al. 1995).

 

Also, there is evidence that detrimental effects on kidney function may

occur at fluoride levels associated

with the " misuse " of fluoridated dentifrice by children (Borke and

Whitford; 1999).

 

Finally, while CDC calls for a normal control range for school

fluoridation systems of up to 6.5-ppm (Water Fluoridation:

 

A manual for water plant operators; 1994) the following relate the

deleterious renal and other effects caused by a bottled mineral

water at 8.5-ppm (Alexandra, et al. 1984; Arlaud, et al. 1984; Noel, et

al. 1985; Camous, et al. 1986; Boivin, et al. 1986; Lantz, et al. 1987;

Welsch, et al. 1990; Haettich, et al. 1991; Nicolay, et al. 1997 and

1999).

 

Some epidemiological studies indicate that men may have a greater

susceptibility to the detrimental effects of fluoride on bone

strength (Karagas, et al. 1996; inter-alia); a comparison of

fluoridated and non-fluoridated areas revealed a significant

increase in osteosarcoma among males under 30-years of age

(Mahoney, et al. 1991); the animal model also produces male

osteosarcomas (Bucher, et

al. 1991); and a gender-specific physiologically based pharmokinetic

model has been developed to describe the absorption, distribution

and elimination of fluoride (Rao, et al. 1995).

 

Testosterone deficiency

is a major risk factor for male osteoporosis (Katznelson, 1998); and

fluoride correlates with decreased testosterone levels (Susheela and

Jethanandani, 1996),

as well as reduced sperm count and motility (Narayana and Chinoy,

1994).

 

In most likelihood, this is the causative factor for reduced fertility

rate in areas of the U.S. having fluoride levels of at least 3-ppm

(Freni, 1994). That is,

based on the deleterious testicular effects in three different

animal models (Chinoy and Sequeira, 1989; Sushella and Kumar, 1991;

Krasowski and Wlostowski, 1992; Kumar and Sushella, 1994 and 1995)

this decrease in the total fertility rate due to ingested fluoride

is paternal in nature.

 

As CDC now " celebrates " the fifty-years of water fluoridation as being

one of the greatest public health advances of

the century, the following have documented very significant

(approximately 50%) decrease in human semen quality (both seminal

volume and mean sperm density)

concomitant with a very significant

(300-400%) increase in testicular cancer over the past fifty-years –

(Carlsen, et al. 1992; Giwercman, et al. 1993; Carlsen, et al. 1995;

Skakkebaek, et al. 1998; Medras and Jankowska, 1999; Sinclair,

2000).

 

While those references assert that this must be due to some (albeit

undetermined) environmental pollutant, the previous mentioned study

showing decreased total fertility rate in the areas of the U.S. with

water fluoride levels of at least 3-ppm (ibid, 1994) has a consensus

p-value of 0.0002 - 0.0004.

 

In addition to being a " reproductive effector " (due to both paternal

and maternal effects) the compound descriptors for sodium-fluoride

in

the NIOSH Registry of Toxic Effects of Chemical Substances (RTECS)

also include " tumorigen " and " mutagen " .

 

The latter is based on more than 40 positive results including the

following -- unscheduled DNA

synthesis and DNA inhibition of human fibroblast; cytogenic analysis

of human fibroblast, human lymphocyte, and other human cells;

mutation in human lymphocyte; and DNA inhibition in human lung.

 

Similarly, another review of genetic toxicity (Zeiger, et al. 1993)

states that gene mutations in human cells were produced in the

majority of cases, and " the weight of the evidence leads to the

conclusion that fluoride does result in increased chromosome

aberrations " .

 

The " painful lower extremity syndrome " from fluoride treatment has

been attributed (O'Duffy, et al. 1986) to stress fractures. An

associated fibromyalgia however, should not be dismissed out of

hand.

 

It is associated with " chronic fatigue syndrome " , and there is a

relationship between chronic fatigue and pineal gland calcification

(Sandyk and Awerbuch, 1994) with the latter consisting of apatite

crystals similar in size and structure to dentin and bone (Nakamura,

et al. 1995).

 

Thus, fluorides potential to acerbate soft-tissue pathologies in

general, deserves further consideration.

 

Similarly, the cognitive difficulties that result from exposure to

fluoride

(Spittle, 1994) are accompanied by general malaise and fatigue;

intolerance to low levels of environmental chemicals is a

polysymptomatic sequela of chronic fatigue, fibromyalgia, etc.

resulting from an immunological

and/or a neurogenic triggering of

somatic symptoms and inflammation (Bell, et al. 1998); and the

earliest subjective symptoms of osteo-fluorosis are arthritic in

nature.

 

Side-effects of fluoride treatment also include gastro-intestinal

problems simply referred to as -- " symptoms " (Riggs, et al.

1990); " intolerance " (Dequeker and Declerick, 1993);

and " complaints " (Lips, 1998).

 

In two separate studies, the comparative results

between patients receiving fluoride treatment for 3-12 months (Das,

et al. 1994) and those having documented osteo-fluorosis (Dasarathy,

et al. 1996) were identical - 70% endoscopic abnormalities, 70-90%

histologic chronic atrophic gastritis; and 100% microscopic

abnormalities such as loss of microvilli.

 

Moreover, these affects were also qualitatively similar to a study

(Gupta, et al. 1992) that correlated non-ulcer dyspepsia with ingested

fluoride level. As

expected, symptoms occurring at the (RTECS) human acute TDLo dosage

of only 214 ug/kg are gastrointestinal.

 

Similar to curing osteoporosis, fluoride has been proposed as a

preventive measure (sic) against Alzheimer's Disease (AD) based on

the presumption that by direct competition in the gut, fluoride

would

decrease aluminum uptake (Kraus and Forbes, 1992).

 

Rather, such antagonism (Li, et al. 1990) is due to the formation of

aluminum-

fluoride complex (Li, et al. 1991). That fluoride potentiates neuro-

toxicity of aluminum has been substantiated (van der Voet, et.al.

1999) -- consisting of interference with neuronal cytoskeleton

metabolism.

 

Aluminum accumulations have been found in nuclei of the

paired-helical filament (PHF) containing neurons in the brains of

both AD patients and elderly normal controls (Shore and Wyatt, 1983)

but as no elevations of aluminum were found in serum or

cerebrospinal

fluid of AD patients, aluminum alone is not the cause – rather,

aluminum in PHF bearing neurons is simply a " marker " .

 

Fluoride had been deemed to be a potent stimulator of bone formation

(Farley, et al. 1983), but most recent work indicates that the mitogenic

effect

on osteoblasts is due to fluoro-aluminate (Caverzasio, et al. 1997;

Susa, et al. 1997) -- while another model claims the mitogenic

action is non-specific (Lau and Baylink,1998).

 

In the animal model, 0.5-ppm aluminum-fluoride for one-year resulted in

decreased neuronal density

and " necrotic-like " brain-cells (Varner, et al. 1998). Also,

fluoride decreases protein content of brain tissue (Shashi, et al.

 

1994) with 7-months of 30-ppm fluoride resulting in a 10% decrease in

total brain phospholipid content (Guan, et.al. 1998)

– as well as (biphasic) changes in brain levels of coenzyme-Q (Wang, et

al. 1997).

 

Osteo-fluorosis is endemic in certain regions of China (Dasheng and

Cutress, 1996) with detrimental effects of fluoride on the IQ of

children now being documented (Yang, et al. 1994; Li, et al. 1995).

 

Just as ingested fluoride has a deleterious effect on bone, the same

is true for developing teeth.

 

Peer Review Journal References Cited in the Text – with more than

80% of them being published within the past ten-years

 

Akapa, et al. (1997). Dental fluorosis in 12-15-year-ol rural

children exposed to fluorides from well drinking water in the Hail

region of Saudi Arabia. Community Dent Oral Epidemiol; 25(4): 324-

327.

 

Alexandre, et al. (1984). Fluoride poisoning caused by Vichy Saint-

Yorre water. [title only; article in French]. Presse Med; 13(16);

1009.

 

Alhava, et al. (1980). The effect of drinking water fluoridation on

the fluoride content, strength and mineral density of human bone.

Acta Orthop Scand; 51(3): 413-420.

 

Angelillo, et al. (1999). Caries and fluorosis prevalence in

communities with different concentrations of fluoride in the water.

Caries Res; 33(2):114-122.

_________________

 

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DietaryTi-

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