Fluoride: Friend or Foe?

Fluoride is good for you. . .it prevents tooth decay, right? Tooth decay trends tracked by the World Health Organization from 1970 to the present show that the incidence of decayed, missing, or filled teeth has been steadily in decline with each passing year in the U.S., France, Germany, Japan, Italy, Sweden, Finland, Denmark, Norway, The Netherlands, Northern Ireland, Austria, Belgium, Portugal, Iceland, and Greece. Better oral hygiene and improved dentistry are the most likely reasons for this
upswing in dental health. But it certainly can't be attributed to the fluoride. Because out of all of those countries, only one adds fluoride to the public water supply: the United States.

Let’s take a closer look at this halogen, which is closely related to the highly toxic element chlorine used as an antibiotic in many community water supplies. We know that chlorine, for example, with the same outer electron configuration and therefore very similar chemistry to fluorine, causes over 10,000 cases of cancer each year due to its addition to our water supplies. This includes 9% of bladder cancer and 18% of rectal cancer based on meta-analysis of ten major studies between 1978 and 1987. 25% of bladder cancer among non-smokers is linked to chlorine and its byproducts, called trihalomethanes, which are produced when it reacts with organic matter. Chlorine has also been linked to heart attacks, diabetes, kidney stones, gout, and possibly multiple sclerosis and muscular dystrophy.

Fluoride has similar characteristics, but is so strongly binding, that there is no medical way to chelate it out of the body, leaving homeopathic treatment as the only solution at this time. A number of studies have linked fluoride to as many as 10,000 cancer deaths each year, with a high incidence of bone cancer among men exposed to fluoride. In animal trials, fluoride has been shown to enhance the brain's absorption of aluminum, a toxin shown to contribute to Alzheimer's disease. Several osteoporosis studies have associated hip fractures with fluoride intake.

According to the Handbook of Clinical Toxicology of Commercial Products, fluoride is more toxic than lead and only slightly less toxic than arsenic. And it accumulates in the body. A byproduct of the phosphate fertilizer industry, over 140,000 tons are put into our water every year, not to mention what is added to toothpaste and vitamins. Fluoride gels used for fluoride treatment in dental offices contain potentially lethal doses of fluoride if swallowed. Even a tube of toothpaste, with up to 1.5 grams of fluoride, can be a lethal dose to a young child. Unfortunately, the ADA will only give its seal of approval to those products that do contain fluoride, and any reversal of this position would serve to trigger an increase in lawsuits on the issue. Suits have already been filed in America as well as Canada, England and Australia. A family in New York was awarded $750,000 for the death of their 3-year-old child who accidentally swallowed fluoride gel during a dental treatment. An antidote for acute fluoride poisoning is to drink milk, which changes the form of the fluoride to a safer form, calcium fluoride. This knowledge could have saved the child’s life. Symptoms of fluoride allergy or toxicity include restlessness, insomnia, nausea, swollen lips, calcification of tendons, cataracts and even triggering Down’s Syndrome (Trisomy 21) due to interference with chromosomal function. Increased sensitivity can be due to kidney stress, autoimmune processes, immunodeficiency, diabetes and heart problems.

High Risk/No Benefits

Fluoride, first of all, does not reduce or prevent tooth decay. All of the recent large studies agree on this point. A study of 60,000 children in New Zealand showed that fluoridation had no significant effect on decay in permanent teeth. The largest study in this country was performed by the United States Public Health Service on 39,000 children, and found virtually the same rate of decayed, missing and filled permanent teeth in both fluoridated and non fluoridated areas all around the country. Going a step further, the Journal of the Canadian Dental Association found in 1987, “school districts recently reporting the highest caries-free rates in the province were totally unfluoridated.” The Pasteur Institute in France and the Nobel Institute in Sweden both agree that fluoride offers little or no prevention of dental caries, and that potential health risks outweigh any benefit.

Fluoride drops and tablets are not even approved by the FDA as safe or effective. Nor has the FDA ever labelled fluoride a proven cavity fighter. The EPA classifies fluoride as a contaminant. In fact, fluoride weakens and destroys bone tissue by a disease process called fluorosis. Dental fluorosis is actually visible as mottled white or brown spots on the teeth where the fluoride has prevented the enamel of the adult teeth from crystallizing. This represents one of the first obvious signs of fluoride toxicity, ranging from subtle chalky blotches to severe rusty-looking stains with pitting and associated brittleness of the teeth. Dental fluorosis is found in up to 84% of children in fluoridated areas around the country. Children age 12 and under are the most at risk. This problem has been known since 1931, when it came out as headline news.

By 1939, the American Water Works Association recommended that drinking water should not exceed 0.1 ppm. Then, the US PHS found that as fluorosis increased with higher levels of fluoride in the water, the rate of tooth decay seemed to drop by 50%. What they didn’t know, and still don’t understand, is that this was due to a shift in the biophysical terrain from Phase 2 (bacterial, such as tooth decay) to Phase 1 (degenerative, such as fluorosis and cancer). Tests were set up in four towns to increase their water’s fluoride content to 1 ppm, and preliminary results of the 10 year trial period showed a 60% reduction in cavities, as the people’s terrain started shifting to Phase 1. On June 1, 1950, just half way through the study, the US PHS decided to go ahead and endorse the “safety and effectiveness of artificial fluoridation.”

Even if we were only exposed to fluoride from 1 ppm added to our water, 10% of us would still get fluorosis. Since we have not consented to this, it is legally considered compulsory medication. Unfortunately, 50% of Americans are exposed to this level in our water, plus we are exposed to fluoride from other sources as well, including processed foods, drinks, baby formulas, fluoride supplements, dental treatments, dental hygiene products, fruits and vegetables grown with phosphate fertilizers, and even fluoride-based insecticides and fungicides. At 2 ppm in the water alone, 50% of the population develops fluorosis, and 95% get it at just 3 ppm. Non-organic grape juice has been measured with over 7.7 ppm of fluoride residue from insecticides and fungicides. Just 3 ounces a day of this juice by itself would provide the full dosage conventionally recommended by the proponents of fluoridation for a child under the age of 6. Health Effects of Ingested Fluoride states “In areas where the water is optimally fluoridated (1 ppm), it is inappropriate to prescribe the use of fluoride supplements.” Nevertheless, many pediatricians and dentists still do so, adding more fluoride to the so-called ‘optimal’ dosage of this toxin. The rate of dental fluorosis continues to rise. According to Professor Myers of the University of Rochester, “Dental fluorosis (mottled enamel) can be regarded as perhaps the best example of a completely preventable disease of the teeth.”

Fluorosis is visible in the teeth, but affects other bone tissue as well. In fact, the rate of hip fractures increases by 86% in men and women who live in areas with fluoridated water over 0.11 parts per million. Four studies in the Journal of the American Medical Association have shown increased hip fractures from fluoride. The New England Journal of Medicine has also reported research, done at the Mayo Clinic, showing that fluoride treatment for osteoporosis increased bone fractures and bone fragility.

Fluoride acts as an antibiotic, killing bacteria by poisoning their enzymes. This is detrimental to our friendly intestinal flora. Even more significantly, fluoride blocks vital enzymes in the mitochondria as well, interfering with cellular energy production. European studies have shown that fluoride shifts the body into Phase 1 (Low Energy) terrain, setting it up for cancer and degenerative disease. Fluoride has been linked to kidney and bladder disease, bone malformation, arthritis, skin disease, aortic calcification, thyroid dysfunction including hypothyroidism, obesity, birth defects, cancer and immunodeficiency.

Fluoride and your Brain

The union which represents all the workers at the EPA has stated “our members review of the body of evidence over the last eleven years including animal and human epidemiological studies, indicate a causal link between fluoride/fluoridation and cancer, genetic damage, neurological impairment and bone pathology. Of particular concern are recent epidemiological studies linking fluoride exposures to lower I.Q. in children.

A recent study published in Brain Research showed that sodium fluoride at levels equivalent to water fluoridated at 1 ppm caused brain damage similar to that found in Alzheimer’s and other dimentia patients. Aluminum accumulation in brain tissue was found to be increased 200 times by the presence of fluoride!

Cancer

Fluoride not only weakens bone tissue, making it brittle, but also increases bone cancer according to findings of the Safe Water Foundation, the New Jersey Department of Health and the National Cancer Institute. Fluoride causes other cancers, too, increasing the cancer rate a full 5% when it is added to the community water supply. This means about 10,000 Americans die each year from cancer caused by fluoride added to our water supply, according to the research of Dr. Dean Burk, the former Chief Chemist at the National Cancer Institute. This is just as bad as the statistic for its closest relative, chlorine. Even half the level of fluoride added to our water supplies has been shown to significantly increase genetic damage, according to a study by Procter and Gamble. A 1988 study by Argonne National Laboratory demonstrated “the ability of fluoride to transform normal cells into cancer cells.” Research at Batelle Research Institute linked fluoride to liver cancer, oral tumors and bone cancer in animal experiments. Even The National Institute of Environmental Health Sciences stated in 1993 that “In cultured human and rodent cells, the weight of the evidence leads to the conclusion that fluoride exposure results in increased chromosome aberrations.”

Playing: Politics with our Health

Dr. William Marcus, a Senior Scientist at the Office of Drinking Water was fired in 1990 when he called for an independent review board to investigate fluoride. He eventually won in a law suit against the Environmental Protection Agency, and he is not alone in questionning the conventional ‘wisdom’ of fluoridation.

Dr. Richard G. Foulkes, author of a 1973 Canadian government report recommending mandatory fluoridation has now compiled a 2,000 page report reversing his recommendation and supporting his new position with research-based evidence. He claims to have been “conned” into his original position of support for fluoridation by misleading information fed to him by a powerful fluoridation lobby. The references he was originally given excluded studies that showed fluorides ineffectiveness at preventing tooth decay, as well as those showing the health consequences of fluoridation.

Zev Remba, the Washington Bureau Editor for the Academy of General Dentistry’s monthly publication, AGD Impact, concurrs, citing fluoridation promoters’ “unwillingness to release any information that would cast fluorides in a negative light.”

Edward Groth III wrote his 1973 Ph.D. thesis at Stanford on fluoridation and found that almost all literature reviews published on the topic were geared to promote fluoridation rather than to objectively examine the evidence.

Many studies never get published because they go against the prevailing ‘conventional wisdom’ that fluoride is good. For example, Dr. Harold Warner, professor emeritus of biomedical engineering at Emory University Medical School, together with Sohan L. Manocha tried to publish a study in JAMA in 1974 showing enzyme changes in monkeys drinking fluoridated water. Reviewers rejected the manuscript with comments like “I would recommend that this paper not be accepted for publication at this time” because “this is a sensitive subject and any publication in this area is subject to interpretation by anti fluoridation groups.” After their study was rejected for publication, the authors were told by their department head not to submit it for publication in any other U.S. journal because of a warning received from the NIDR. They eventually had to publish in a foreign journal.

Dr. H. Trendley Dean, known as the “father of fluoridation” has been forced to admit more than once in court that his statistics favoring fluoridation were not valid. He also admitted that critiques of the research were omitted, as were several studies which found no reduction in tooth decay with fluoridation.

In 1980, Brian Dementi, who was toxicologist at the Virginia Department of Health, wrote a comprehensive report on “Fluoride and Drinking Water” which examined the possible health risks. The report, the only one the department has ever produced on the topic of fluoride, has since been deleted from the department’s library.

John A. Colquhoun, former chief dental officer at the Department of Health in Aukland, New Zealand found that there was no benefit from fluoridation in that country in 1982, but the Department refused to give permission for him to publish the findings.

Robert J. Carton, environmental scientist at EPA, states that the EPA’s 1985 scientific assessment of fluoride’s health risks “omits 90% of the literature on mutagenicity, most of which suggests fluoride is a mutagen.”

A number of dentists who have testified on the risks of fluoridation have been reprimanded by their state dental officers. In addition, both the ADA and the PHS have attacked either the work or the character of investigators who uncover problems with fluoride in their research. For example, as far back as 1956, the ADA published false allegations about the work of the late George L. Waldbott, founder and chief of allergy clinics in four hospitals. These same allegations were still being quoted 3 decades later.

The Public Health Service, responsible for most of the funding for fluoridation research, has been publicly committed to the promotion of fluoridation since June of 1950. Any research suggesting harm from fluoride would be politically damaging to the agency and its budget. This could present a conflict of interest.

In 1991, the National Federation of Federal Employees who staff the EPA charged both EPA and the Surgeon General’s office with falsifying information on the risks of fluoride. They renounced the use of fluoride as an unsafe practice.

In 1992, The EPA tried to fire a high ranking toxicologist for talking about the link between fluoride and cancer and the downgrading “in almost all instances” of research data definitely linking fluoride to tumors in the National Toxicology Program.

Fluoridation: status around the world

The United States have the third highest rate of fluoridation of any nation, and the highest rate of hip fractures in the world. After more than 40 years of fluoridation, there is no evidence that Americans have less tooth decay than those in nations who reject fluoridation completely, including Denmark, Belgium, Netherlands, Norway, Sweden, Portugal, Poland, Romania, Germany, Austria, Bulgaria, Hungary, Iran, Finland, France, Italy, Spain, India, Greece, Indonesia and Japan. In fact, the only other major countries using large amounts of fluoridation are Canada, New Zealand, Australia and Ireland.

Why don’t all countries fluoridate their water? In continental Western Europe, less than 1% of the population drinks fluoridated water. The Netherlands tried fluoridation for 10 years and then stopped. West Germany tried it in a few towns and then gave it up, too, for both legal and health reasons. France’s Chief Council of Public Health rejected fluoridation in 1980 due to concerns that it could harm human health. Denmark’s minister for the environment recommended against fluoridation because no long term studies looked at human health effects other than teeth. Finland rejected fluoridation after testing it for more than 20 years, when they found women with high fluoride content in their bones. Fluoride replaces calcium in bone tissue.

As the word gets out about fluoride, watch for labels to reduce the size of the box promoting “Fluoride” on the label, or even hide it in the middle of the list of ingredients with no additional notice of its presence. This way, they can still maintain their ADA approval. Also, they are not permitted to reduce the dosages to lower levels without getting FDA approval as a new drug, so this is unlikely. It is best to just avoid fluoride, or use it in non-toxic homeopathic form, such as Calcarea fluorica. As Paracelsus said in the 16th century of the Christian era, “All substances are poisons; there is none that is not a poison. The right dose differentiates a poison and a remedy.”

Improve your diet and nutrition to prevent cavities, and rebuild dental and bone health with microcrystalline hydroxyapatite. Also, drink and cook with filtered water. Starfire’s countertop water filter removes over 99% of the fluoride from tap water when it is new, and still removes 91% when it has filtered over 28,000 gallons, making it the most cost-effective way to remove fluoride (as well as chlorine and other toxins).

(for 34 footnotes, see print version)

Why is the CDC Covering Up a Fifty Year Old Mistake?

Roger D. Masters (Research Professor, Dartmouth College)

Controversy over "fluoridating" public water supplies has been on the agenda for half a century. Although the specific chemicals in use raise genuine scientific questions, most proponents (from the Surgeon General to the American Dental Association) and critics talk about "fluoridation" without discussing the difference between sodium fluoride, familiar in toothpaste, and fluosilicic acid or sodium silicofluoride (jointly called "silicofluorides"), which are the main chemicals used for water fluoridation in the U.S. Does the difference matter? If so, why does a long-delayed CDC report on fluoride treatments carefully list the chemicals in fluoridated gels and mouthwash, but refuse to mention the chemicals used in our water supplies?

Water fluoridation was begun in the mid 1940's as a ten year experiment to see if drinking-water with sodium fluoride would reduce tooth decay. All tests of safety were conducted on sodium fluoride. In 1950, however, the Public Health Service authorized the substitution of silicofluorides, even though they had never been tested for effects on health and behavior. Today, over 90% of fluoridated water (delivered to over 140 million Americans) is treated with one of the silicofluorides.

The switch to silicofluorides about 50 years ago may have been an enormous mistake. Three years of intensive research, supported by the Earhart Foundation, has indicated that

1. Silicofluorides have never been tested for health and safety, and the EPA admits it now has no information on the effects of "chronic exposure" to water treated with them.
2. Silicofluorides do not dissociate completely after injection in public water supplies and their biochemical effects are not benign.
3. Extensive data analysis (based on three large samples of over 400,000 children) reveals that where silicofluorides are in use, children absorb significantly higher levels of lead from environmental sources (such as old housing).
4. Additional studies show that where silicofluorides are in use, there are higher rates of behavioral problems that have been linked to lead toxicity (including hyperactivity and other learning disabilities, substance abuse, and violent crime). These findings are based on a "cumulative loading" model of environmental risk factors.

The CDC and EPA have constantly refused to support objective scientific testing and have apparently engaged in a cover-up of data suggesting toxicity and harmful effects due to silicofluorides. The pattern evident in prior reports and funding decisions is especially noteworthy in the long-delayed CDC report on "Recommendations for Using Fluroide to Prevent and Control Dental Caries in the United States" (MMWR, Aug. 17, 2001, 50 [RR14] 1-42). This document is silent on the different health and behavioral effects of silicofluoride treated water compared to that treated with sodium fluoride. Although the report identifies the specific chemicals used to add fluoride to mouth rinse (sodium fluoride), dietary fluoride supplements (sodium fluoride), gel and foam (acidulated phosphate fluoride, sodium fluoride, or stannous fluoride) or fluoride varnish (sodium fluoride or difluorsilane), there is no mention of the specific chemicals used to fluoridate public water supplies or toothpaste (the two principal sources of fluoride for caries control).

Given the foregoing information, informed observers suspect that the CDC intentionally omitted information to "cover up" the fact that silicofluorides, although used in over 90th of water fluoridation in the U.S., have never been subjected to the tests conducted on sodium fluoride or other health products and medicines. Some CDC personnel know the research questioning silicofluorides, and in one case attended a presentation of research on their dangers.

It is time to discuss openly a toxin that could well contribute to higher rates of hyperactivity (ADHD) and crime in many American communities. Why should we allow bureaucrats to block discussion of the differences between either fluosilicic acid or sodium silicofluoride (toxic byproducts of manufacturing phosphate fertilizer as well as nuclear fuel and warheads) and sodium fluoride? Since silicofluorides have never been tested, shouldn't there be a moratorium on their use until their safety has been proven? If you live in Manhattan, you can choose non-fluoridated toothpaste but not non-fluoridated water. It's time for Congressional hearings on an issue that could help our children at virtually no cost (except for lost revenue to some chemical corporations and embarrassment to the CDC, EPA, and American Dental Association).

References:

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.
Arlaud, et al. (1984). Osteomalacia disclosing bone fluorosis caused
by regular consumption of Vichy Saint-Yorre mineral water. [title
only; article in French]. Presse Med; 13(39); 2393-2394.
Arnala, et al. (1985). Effects of fluoride on bone in Finland:
histomorphometry of cadaver bone from low and high fluoride areas.
Acta Orthop Scand; 56(2): 161-166.
Balena, et al. (1998). Effect of different regimens of sodium
fluoride treatment for osteoporosis on the structure, remodeling and
mineralization of bone. Osteoporos Int: 8(5): 428-435.
Bell, et al. (1998). Serum neopterin and somatization in women with
chemical intolerance. Neuropsychobiology; 38(1): 13-18.
Bodier-Houlle, et al. (1998). First experimental evidence for human
dentin crystal formation involving conversion of octacalcium
phosphate to hydroxyapitite. Acta Crystallogr D Biol Crystallogr; 54
(2 ? Pt 6): 1377-1381.
Boivin, et al. (1986). Histophometric profile of bone fluorosis
induced by prolonged ingestion of Vichy Saint-Yorre water.
Comparison
with bone fluorine levels. Pathol Biol; 43(1): 33-39.
Boivin, et al. (1988). Fluoride content in human iliac bone: results
in controls, patients with fluorosis, and osteoporotic patients
treated with fluoride. J Bone Miner Res; 3(5): 497-502.
Boivin, et al. (1989). Skeletal fluorosis: histomorphometric
analysis
of bone changes and fluoride content in 29 patients. Bone; 10(2): 89-
99.
Borke and Whitford (1999). Chronic fluoride ingestion decreases 45Ca
uptake by rat kidney membranes. J Nutr; 129(6): 1209-1213.
Bucher, et al. (1991). Results and conclusions of the National
Toxicology Program's rodent carcinogenicity studies with sodium
fluoride. Int J Cancer; 48(5): 733-737.
Camous, et al. (1986). [title only; article in French]. Hypokalemia
with severe rhythm disorders induced by Vichy water. Presse Med; 15
(44): 2212-2213.
Carlsen, et al. (1992). Evidence for decreasing quality of semen
during past 50 yrs. BMJ; 305(6854): 609-613.
Carlsen, et al. (1995). Declining semen quality and increasing
incidence of testicular cancer: is there a common cause? Environ
Health Perspect; 103 (Suppl 7): 137-139.
Carter and Beaupre (1990). Effects of fluoride treatment on bone
strength. J Bone Miner Res; 5(suppl 1): 177-184.
Caverzasio, et al. (1997). Mechanism of the mitogenic effect of
fluoride on osteoblast-like cells: evidences for G protein-dependent
tyrosine phosphorylation process. J Bone Miner Res; 12(12): 1975-
1983.
Chinoy and Sequeiera (1989). Effects of fluoride on
histoarchitecture
and reproductive organs in male mouse. Reprod Toxicol; 3(4): 261-267.
Clark (1994). Trends in prevalence of dental fluorosis in North
America. Community Dent Oral Epidemiol; 22(3): 148-152.
Cisternas, et al. (1994). Dietary ingestion of fluoride and caries
prevalence in preschool and school children in cities with different
fluoride content in the drinking water and diet. Rev Med Chil; 122
(4): 459-464.
Danielson, et al. (1992). Hip fractures and fluoridation in Utah's
elderly population. JAMA; 268(6): 746-748.
Das, et al. (1994). Toxic effects of chronic fluoride ingestion on
the upper gastrointestinal tract. J Clin Gastroenterol; 18(3): 194-
199.
Dasarathy, et al. (1996). Gastroduodenal manifestations in patients
with skeletal fluorosis. J Gastroenterol; 31(3): 333-337.
Dasheng and Cutress (1996). Endemic fluorosis in Guizhou Province,
China. World Health Forum; 17(2): 173-174.
de Liefde (1998). The decline of caries in New Zealand over the past
40 years. N Z Dent J; 94(417): 109-113.
Dequeker and Declerick (1993). Fluor in the treatment of
osteoporosis: an overview of thirty years of clinical research.
Schweiz Med Wochenschr; 123(47): 2228-2234.
Diesendorf, et al. (1997). New evidence on fluoridation. Aust N Z J
Public Health; 21(2): 187-190.
Einarsdottir and Bratthall (1996). Restoring oral health. On the
rise
and fall of dental caries in Iceland. Eur J oral Sci; 104(4 Pt 2):
459-469.
Evans, et al. (1996). The effect of fluoridation and social class on
caries experience in 5-year-old Newcastle children in 1994 compared
with results over the previous 18 years. Community Dent Health; 13
(1): 5-10.
Farley, et al. (1983). Fluoride directly stimulates proliferation
and
alkaline phosphatase activity of bone-forming cells. Science; 222
(4621): 330-332.
Fejerskov, et al. (1994). Dental tissue effects of fluoride. Adv
Dent
Res; 8)1): 15-31.
Feskanich, et al. (1998). Use of toenail fluoride levels as an
indicator for the risk of hip and forearm fractures in women.
Epidemiology: 9(4): 412-416.
Fratzl, et al. (1994). Abnormal bone mineralization after fluoride
treatment in osteoporosis: a small-angle x-ray-scattering study. J
Bone Miner Res; 9(10): 1541-1549.
Fratzl, et al. (1996). Effects of Na-F and alendronate on the bone
mineral in minipigs: small-angle x-ray scattering and backscattered
electron imaging study. J Bone Miner Res; 11(2): 248-253.
Frencken, et al. (1992). Exposure to low levels of fluoride and
dental caries in deciduous molars of Tanzanian children. Caries Res;
26(5): 379-383.
Freni (1994). Exposure to high fluoride concentrations in drinking
water is associated with decreased birth rates. J Toxicol Environ
Health; 42(1): 109-121.
Gerstner, et al. (1983). Bilateral fractures of femoral neck in
patients with moderate renal failure receiving fluoride for spinal
osteoporosis. Br Med J (Clin Res Ed); 287(6394): 723-725.
Gitomer, et al. (2000). A comparison of fluoride bioavailability
from
a sustained-release NaF preparation (Neosten) and other fluoride
preparations. J Clin Pharmacol; 40(2): 138-141.
Giwercman, et al. (1993). Evidence for increasing incidence of
abnormalities of the human testis: a review. Environ Health
Perspect;
101(Suppl 2): 65-71.
Grynpas (1990). Fluoride effects on bone crystals. J Bone Miner Res;
5
(suppl 1): 169-175.
Guan, et al. (1998). Influence of chronic fluorosis on membrane
lipids in rat brain. Neurotoxicol Teratol; 20(5): 537-542.
Gupta, et al. (1992). Fluoride as a possible aetiological factor in
non-ulcer dyspepsia. J Gastroentero Hepatol; 7(4): 355-359.
Gupta, et al. (1993). Skeletal scintigraphic findings in endemic
skeletal fluorosis. Nucl Med Commun; 14(5): 384-390.
Haettich, et al. (1991). Magnetic resonance imaging fluorosis and
stress fractures due to fluoride. Rev Rhum Mal Osteoartic: 58(11):
803-808
Haimanot (1990). Neurological complications of endemic skeletal
fluorosis with special emphasis on radiculo-myelopathy. Paraplegia;
28
(4): 244-251.
Hartshorne, et al. (1994). The relationship between plaque index
scores, fluoride content of plaque, plaque pH, dental caries
experience and fluoride concentration in drinking water in group of
primary school children. J Dent Assoc S Afr; 49(1): 5-10.
Haugejorden (1997). Using the DMF gender difference to assess
the "major" role of fluoride toothpastes in the caries decline in
industrialized countries: a meta-analysis. Community Dent Oral
Epidemiol; 24(6): 369-375.
Hedlund and Gallagher (1989). Increased incidence of hip fracture in
osteoporotic women treated with sodium fluoride. J Bone Miner Res: 4
(2): 223-225.
Hillier, et al. (1996). Water fluoridation and osteoporotic
fracture.
Community Dent Health; 13(2): 63-68
Ibrahim, et al. (1997). Caries and dental fluorosis in a 0.25 and a
2.5 ppm fluoride area in the Sudan. Int J Paediatr Dent; 7(3): 161-
166.
Ismail, et al. (1993). Should the drinking water of Truro, Nova
Scotia, be fluoridated ? Community Dent Oral Epidemiol; 21(3): 118-
125.
Ismail and Messer (1996). The risk of fluorosis in students exposed
to a higher than optimal concentration of fluoride in well water. J
Public Health Dent; 56(1): 22-27.
Ittel, et al. (1992). Effect of fluoride on aluminum-induced bone
disease in rats with renal failure. Kidney Int; 41(5): 1340-1348.
Jacobsen, et al. (1992). The association between fluoridation and
hip
fracture among white women and men aged 65-years or older: a
national
ecologic study. Ann Epidemiol; 2(5): 617-626.
Karagas, et al. (1996). Patterns of fracture among United States
elderly: geographic and fluoride effects. Ann Epidemiol: 6(3): 209-
216.
Kassabi, et al. (1981). Comparison sodium and stannous fluoride
nephrotoxicity. Toxicol Lett; 7(6): 463-67
Katznelson (1998). Therapeutic role of androgens in treatment of
osteoporosis in men. Ballieres Clin Endocrinol Metab; 12(3): 453-470.
Kleerekoper, et al. (1991). Randomized trial of sodium fluoride as
treatment for post-menopausal osteoporosis. Osteoporos Int; 1(3):
155-
161.
Kleerekoper (1996). Fluoride and the skeleton. Crit Rev Clin Lab
Sci;
33(2): 139-161.
Kobayashi, et al. (1992). Caries experience in subjects 18-22 years
of age after 13 years discontinued water fluoridation in Okinawa.
Community Dent Oral Epidemiol; 20(2): 81-83.
Kono (1994). Health effects of fluorine and its compounds. Nippon
Eiseigaku Zasshi; 49(5): 852-860.
Kopp and Robey (1990). Sodium fluoride does not increase human bone
cell proliferation or protein synthesis in vitro. Calcif Tissue Int;
47(4): 221-219.
Kotha, et al. (1998). Varying the mechanical properties of bone
tissue by changing the amount of its structurally effective bone
mineral content. Biomed Mater Eng; 8(5-6): 321-334.
Kurttio, et al. (1999). Exposure to natural fluoride in well water
and hip fracture: a cohort analysis in Finland. Am J Epidemiol; 150
(8): 817-824.
Krasowski and Wlostowski (1992). The effect of high fluoride intake
on tissue trace elements and histology of testicular tubules in the
rat. Comp Biochem Physiol; 103(1): 31-34.
Kraus and Forbes (1992). Aluminum, fluoride and prevention of
Alzheimer's disease. Can J Public Health; 83(2): 97-100.
Krishnamachari (1989). Skeletal fluorosis in humans: a review of
recent progress in the understanding of the disease. Prog Food Nutr
Sci; 10(3-4): 279-314
Kumar and Susheela (1994). Ultrastructural studies of
spermatogenesis
in rabbit exposed to chronic fluoride toxicity. Int J Fertil
Menopausal Stud; 39(3): 164-171.
Kumar and Susheela (1995). Effects of chronic fluoride toxicity on
morphology of ductus epididymis and maturation of spermatozoa of
rabbit. Int J Exp Pathol; 76(1): 1-11.
Kunzel and Fischer (1997). Rise and fall of caries prevalence in
German towns with different F concentrations in drinking water.
Caries Res; 31(3): 166-173.
Kunzel and Fischer (2000). Caries prevalence after cessation of
water
fluoridation in La salud, Cuba. Caries Res; 34(1): 20-25.
Lance, et al. (1987). Fluoride-induced chronic renal failure. Am J
Kidney Dis; 10(2): 136-139.
Lau and Baylink (1998). Molecular mechanism of action of fluoride on
bone cells. J Bone Miner Res; 13(11): 1660-1667.
Li, et al. (1990). An acute experimental study on combination of
aluminum and fluorine in various ratios. Hua Hsi I Ko Ta Hsueh Hsueh
Pao; 21(4): 440-443.
Li, et al. (1991). Aluminum and fluorine absorption in a perfusion
system of rat small intestine in vivo. Hua Hsi I Ko Ta Hsueh Hsueh
Pao; 22(2): 189-191
Li, et al. (1995). Effect of fluoride exposure on intelligence in
children. Fluoride; 28(4): 189-192.
Lian and Wu (1986). Osteoporosis -- an early radiographic sign of
endemic fluorosis. Skeletal Radiol; 15(5): 350-353.
Limeback (1994). Enamel formation and the effects of fluoride.
Community Dent Oral Epidemiol; 22(3): 144-147.
Lips (1998). Fluoride in osteoporosis: still an experimental and
controversial treatment. Ned Tijdchr Geneeskd: 142(34): 1913-1914.
Lundy, et al. (1995). Histomorphic analysis iliac crest bone
biopsies
in placebo-treated vs fluoride-treated subjects. Osteroporos Int; 5
(2): 115-129
Mahoney, et al. (1991). Bone cancer incidence rates in NY State:
time
trends and fluoridated drinking water. Am J Public Health; 81(4):475-
479
Mann, et al. (1990). Fluorosis and dental caries in 6-8-year-old
children in a 5 ppm fluoride area. Community Dent oral Epidemiol; 18
(2): 77-79.
Marumo and Li (1996). Renal disease and trace elements. Nipon
Rinsho;
54(1): 93-98.
Medras and Jankowska (1999). The deterioration of the parameters of
the human semen: myth or reality? Ginekol Pol; 70(3): 155-160.
Melton (1990). Fluoride in the prevention of osteoporosis and
fractures. J Bone Miner Res; 5(suppl 1): 163-176.
Meunier, et al. (1998). Fluoride salts are no better at preventing
new vertebral fractures than calcium-vitamin-D . Osteoporos Int; 8
(1): 4-12.
Miyazaki and Morimoto (1996). Changes in caries prevalence in Japan.
Eur J oral Sci; 104(4 Pt 2): 452-458.
Mohr (1990). Fluoride effect on bone formation: an overview.
Tandlaegbladet; 94(18): 761-763.
Moss, et al. (1999). Association of dental caries and blood lead
levels. JAMA; 281(24): 2294-2298.
Mrabet, et al. (1995). Spinal cord compression in bone fluorosis.
Apropos of 4 cases. Rev Med Interne; 16(7): 533-535.
Nadanovsky and Sheiham (1995). Relative contribution of dental
services to the changes in caries level of 12-year-old children in
18
industrialized countries in the 1970s and early 1980s. Community
Dent
Oral Epidemiol; 23(6): 331-339.
Nicolay, et al. (1997). Long term follow up of ionic plasma fluoride
level of patients receiving hemodialysis. Clin Chim Acta; 263(1): 97-
104
Nicolay, et al. (1999). Hypercalemia risks in hemodialysed patients
consuming fluoride-rich water. Clin Chim Acta; 281(1-2): 29-36.
Noel, et al. (1985). Risk of bone disease as a result of fluoride
intake in chronic renal insufficiency. Nephrologie; 6(4)L181-185.
O'Duffy, et al. (1986). Mechanism of acute lower extremity pain
syndrome in fluoride treated osteoporotic patients. Am J Med; 80(4):
561-566.
Nakamura, et al. (1995). Ultrastructure and x-ray microanalytical
study of human pineal concentrations. Anat Anz; 177(5): 413-419.
Narayana and Chinoy (1994). Reversible effect of sodium fluoride
ingestion on spermatozoa of rat. Int J Fertil Menopausal Stud; 39
(6);
337-346
Okazaki, et al. (1985). Promotion of bone dissolution by excessive
fluoride in acidic buffer. Biomaterials; 6(4): 277-280.
Rao, et al. (1995). Physiologically based pharmokinetic model for
fluoride uptake by bone. Regul Toxicol Pharmacol; 22(1): 30-42.
Ream (1981). Effects of short-term fluoride ingestion on bone
formation and resorption in rat femur. Cell Tissue Res; 221(2): 421-
430.
Reddy, et al. (1993). Neuro-radiology of skeletal fluorosis. Ann
Acad
Med Singapore; 22(3); 493-500.
Riggs, et al. (1990). Effect of fluoride treatment on fracture rate
in postmenopausal women with osteoporosis. N Engl J Med; 322(12):
802-
809
Riggs, et al. (1994). Clinical trial of fluoride therapy in
postmenopausal osteoporotic women: extended observations and
additional analysis. J Bone Miner Res; 9(2): 265-275.
Sandyk and Awerbuch (1994). Pineal calcification and its
relationship
to the fatigue of multiple sclerosis. Int J Neurosci; 74(1-4): 95-
103.
Seppa, et al. (1998). Caries frequency in permanent teeth before and
after discontinuation of water fluoridation in Kuopio, Finland.
Community Dent Oral Epidemiol; 26(4): 256-262.
Shashi, et al. (1994). Effect of long-term administration of
fluoride
on levels of protein, free amino acids and RNA in rabbit brain.
Fluoride; 27(3): 155-159.
Shore and Wyatt (1983). Aluminum and Alzheimer's disease. J Nerv
Ment
Dis; 171(9): 553-558.
Silva and Ulrich (2000). In vitro sodium fluoride exposure decreases
torsional and bending strength and increases ductility of mouse
femora. J Biomech:; 33(2):231-243.
Sinclair (2000). Male infertility: Nutritional and environmental
considerations. Altern Med Rev; 5(1): 28-38.
Skakkebaek, et al. (1998). Germ cell cancer and disorders of
spermatogenesis: an environmental connection? APMIS; 106(1): 3-11.
Smith (1985; a). Fluoride, teeth and bone. Med J Aust; 143(7): 283-
286.
Smith (1985; b). Fluoride and bone: an unusual hypothesis.
Xenobiotica; 15 (3): 177-186.
Smogorzewski and Massry (1995). Function and metabolism of brain
synaptosomes in chronic renal failure. Artif Organs; 19(8): 795-800.
Soggard, et al. (1994). Marked decrease in trabecular bone quality
after five years of sodium fluoride therapy: assessed by
biomechanical testing of iliac crest bone biopsies in osteoporotic
patients. Bone; 15(4): 393-399.
Soggard, et al. (1995a). Effects of fluoride on rat vertebral body
biomechanical competence and bone mass. Bone; 16(1): 163-169.
Soggard, et al. (1995b). Loss of trabecular bone strength and bone
quality after 5-years of fluoride therapy for osteoporosis. Ugeskr
Laeger; 157(14): 2002-2008.
Sowers, et al. (1991). A prospective study of bone mineral content
and fracture in communities with differential fluoride exposure. Am
J
Epidemiol; 133(7): 649-660.
Spittle. Psychopharmacology of fluoride: a review (1994). Int Clin
Psychopharmacol; 9(2): 79-82.
Srivastava, et al. (1989). Normal ionized calcium, parathyroid
hypersecretion, and elevated osteocalcin in a family with fluorosis.
Metabolism; 38(2): 120-124.
Stein and Granik (1980). Human vertebral bone: relation of strength,
porosity and mineralization to fluoride content. Calcif Tissue Int;
32
(3): 189-194
Susa, et al. (1997). Fluoroaluminate induces pertussis toxin-
sensitive protein phosphorylation: differences in MC3T3-E1
osteoblatic and NIH3T3 fibroblastic cells. Biochem Biophys Res
Commun; 235(3): 680-684.
Susheela and Jethanandani (1996). Circulating testosterone levels in
skeletal fluorosis patients. J Toxicol Clin Toxicol; 34(2): 183-189.
Susheela and Jha (1983). Cellular and histochemical characteristics
of osteoid formed in fluoride poisoning. Toxicol Lett:16(1-2): 35-40.
Susheela and Kumar (1991). A study of the effect of high
concentrations of fluoride on the reproductive organs of male
rabbits, using light and scanning electron microscopy. J Reprod
Fertil; 92(2): 353-360.
Tollefsen, et al. (1995). Fluorosis: experiences based on two cases.
Tidsskr Nor Laegeforen; 115(21): 2648-2651.
Turner, et al. (1995). Fluoride reduces bone strength in older rats.
J Dent Res: 74(8): 1475-1481.
Turner, et al. (1996). High fluoride intakes cause osteomalacia and
diminished bone strength in rats with renal deficiency. Bone;19
(6):595-601
Turner, et al. (1997). Fluoride treatment increased serum IGF-1,
bone
turnover, and bone mass, but not bone strength, in rabbits. Calcif
Tissue Int; 61(1): 77-83.
Uchimoto, et al. (1995). Implication of parathyroid hormone for the
development of hypertension in young spontaneously hypertensive
rats.
Miner Electrolyte Metab; 21(1-3):82-86.
Usada, et al. (1998). Urinary biomarkers monitoring for experimental
nephrotoxicity. Arch Toxicol; 72(2): 104-109.
van der Voet, et al. (1999). Fluoride enhances the effect of
aluminum
chloride on interconnections between aggregates of hippocampla
neurons. Arch Physiol Biochem; 107)1): 15-21.
Varner, et al. (1998). Chronic administration of aluminum-fluoride
and sodium-fluoride to rats in drinking water: alterations in
neuronal and cerebrovascular integrity. Brain Res; 784(1-2): 284-298.
Vignarajah (1993). Dental caries experience and enamel opacities in
children in urban and rural areas of Antigua with different levels
of
natural fluoride in drinking water. Community Dent Health; 10(2):
159-
166.
Waddington and Langley (1998). Structural analysis of proteoglycans
synthesized by mineralizing bone cells in vitro in the presence of
fluoride. Matrix Biol; 17(4):255-268.
Walsh, et al. (1994). Effect of in-vivo fluoride treatment on
ultrasonic properties of cortical bone. Ann Biomed Eng; 22(4): 404-
415.
Wang, et al. (1994). Endemic fluorosis of skeleton: radiographic
features 127 patients. Am J Roentgenol; 162(1): 93-98.
Wang, et al. (1997). Change in coenzyme Q in brain tissue of rats
with fluorosis. Chung Hua Yu Fang I Hsueh Tsa Chih;31(6): 330-33
Wang and Riordan (1999). Fluoride supplements and caries in non-
fluoridated child population. Community Dent Oral Epidemiol; 27(2):
117-123
Welsch, et al. (1990). Iatrogenic fluorosis. 2 cases. Therapie; 45
(5): 419-422.
Whitford and Williams (1986). Fluoride absorption: independence from
plasma fluoride levels. Proc Soc Exp Biol Med; 181(4): 550-554.
Wiktorsson, et al. (1991). Number of remaining teeth among adults in
communities with optimal and low water fluoride concentrations. Sewd
Dent J; 15(6): 279-284.
Yang, et al. (1994). Effects of high iodine and high fluorine on
children's intelligence and the metabolism of iodine and fluorine.
Chung Hua Liu Hsing Ping Hseuh Tsa Chih; 15(5): 296-298.
Zeiger, et al. (1993). Genetic toxicity of fluoride. Environ Mol
Mutagen; 21(4): 309-318.
Zeigler (1991). Fluoride therapy of osteoporosis. Ther Umsch; 48(2):
8490.

:

:Issues  :Solutions  :Biofield  :Training   :Starfire  :Catalog  :Order

For all Claims by this Ministry: wizardofeyez are with the Vacancy of any Claim by any Ministry of this World.  For the Volition of this Ministry is for our Self-Healing of each Body, Mind and Soul with the Freedom of the Communication of all Truth by the Authority and Grace of our Sovereign-King of all Kings of this Kingdom of the Heavens.
:Authorization-© with the Claim of all Rights: U.C.C.~1-207

:SITE-COPYCLAIM-©: 9/8/2001, A.D., with the Freedom against the Egypt-Calendar: G. M. Swartwout©