Drop of Water Onto Surface of Water Fraud at NAS - Is Fluoride a Nutrient?

Water is for everyone, fluoride toxins are not.

Originally published by: fluoridation.com - Calgary


DISCUSSION SECTION: Fluoride 1998;31(3):153-157
Two Unanswered Letters

The following letter received no reply or acknowledgment: [reply later received - see below]

October 15, 1997

Dr. Bruce Alberts, President
National Academy of Sciences
2101 Constitution Avenue, NW
Washington, DC 20418

Dear Dr. Alberts:

As you may be aware, the Dietary Reference Intakes report on calcium, magnesium, phosphorus, vitamin D, and fluoride prepared by the Institute of Medicine of the National Academy of Sciences and scheduled for publication this month, contains a number of recommendations concerning fluoride that are cause for grave concern over their validity for setting public health policy. This concern has been heightened by statements made by speakers and panel members and their responses to queries at the recent September 23rd workshop on the report held at the National Academy of Sciences.

We, the undersigned, regard the problem as so serious that we are requesting you to take immediate steps to delete the fluoride section of the report and to have it re-addressed by a panel that includes members of the scientific community who are not committed to promoting or supporting fluoride use. What follows is a brief summary of the basis for our concern.

At the heart of the matter is whether fluorine, as fluoride (F), should be ranked with Ca, Mg, P, and vitamin D as an essential nutrient. In fact, there is no known essential biochemical role for fluoride in any animal, including humans. The formation of sound, decay-resistant and caries-free teeth as well as strong, sturdy bones, whether in animal or human populations, does not require fluoride, or at least not in more than minuscule, trace amounts. As acknowledged by sources cited in the report, even when a mother's fluoride intake is elevated, her milk is extremely low in fluoride, but owing to prenatal accumulation, her baby excretes more fluoride than it ingests from her milk. This fact clearly indicates that any natural physiological need for fluoride, if indeed any exists, must be exceedingly small and certainly far below that being recommended in the report.

At the September 23rd workshop, as recorded on videotape, fluoride was repeatedly regarded by speakers and panel members as an essential nutrient. But, toward the end, when challenged on this key issue, Dr. Vernon R. Young, Chair of the Standing Committee on the Scientific Evaluation of Dietary Reference Intakes, bluntly stated that fluoride should not be considered as an "essential" component of the diet. Instead, without clarifying the distinction, he insisted that it should be viewed as only a "beneficial element."

The fact that fluoride is incorporated into the mineral matrix of bones and teeth does not make it an essential nutrient. Other elements hardly considered essential, such as lead and cadmium, also accumulate in bones and teeth, and they are not regarded as beneficial. Obviously, if fluoride is not essential in human nutrition, any consideration of it in terms of an "adequate intake" is clearly not appropriate and should not be part of a "dietary reference intakes" report.

An association of fluoride with reduction in dental caries is cited as the basis for recommending the various intakes of fluoride. At the same time, the report acknowledges that most of the anti-caries effect attributed to fluoride occurs by topical exposure, not through systemic ingestion. Moreover, large, whole-population studies not cited in the report (e.g., in New Zealand) show that declines in tooth decay over the last 40-50 years have been occurring independently of fluoride exposure and use, thereby further challenging current arguments for significant benefit from fluoride.

Without question, however, ingestion of even milligram amounts of fluoride during infancy and early childhood can produce the unmistakable toxic effects of dental fluorosis. This disruption of normal enamel formation is stated in the report not to be of "public health significance" if the fluoride concentration in the drinking water is below 2 mg/liter (2 ppm). But reports of disfiguring dental fluorosis with staining and pitting of the enamel in areas with 1-2 ppm fluoride in the drinking water were evidently overlooked, despite the claim at the workshop that the literature review was comprehensive and thorough.

Of even greater concern, in relation to public health, is the proposal in the report that only the early stages of skeletal fluorosis are the appropriate criteria for fluoride intoxication. For this purpose a tolerable upper level ingestion limit of 10 milligrams of fluoride per day for 10 or more years in persons age 9 or older is proposed. But this level of intake is not tolerable, and, according to the sources cited in the report, it can and does lead to crippling skeletal fluorosis (Hodge, 1979). For young adults, assuming 50% retention of ingested fluoride in hard tissues, as stated on page 8-2 of the prepublication copy of the report, an absorbed intake of 10 mg/day amounts to a yearly accumulation of 1.8 grams or over 50 grams after 30 years. At this level debilitating skeletal fluorosis was observed by Raj Roholm in his classic studies of cryolite workers. But before this condition is reached, there are various pre-skeletal phases of fluoride intoxication with serious health implications that arise from much lower levels of intake, especially when calcium and magnesium are marginal, an aspect not considered in the report. Among these manifestations are increased hip-fracture among the elderly from deterioration in bone strength and quality (in agreement with long-term laboratory animal studies), increased osteosarcoma in young males (also demonstrated in male rats), chronic gastrointestinal irritation (reversible with decreased exposure to fluoride), and various neuromuscular disorders whose connection with fluoride has been well confirmed in peer-reviewed publications without convincing refutation. Recent studies showing decreased IQ scores correlating with dental fluorosis (again backed up by laboratory animal research) were also omitted from consideration.

When questioned at the workshop about these omissions, the speakers and the members of the panel became defensive and were unwilling or unable to explain why such findings had been excluded in setting the upper tolerance level of fluoride at 10 mg/day. From the record of some of the committee members' past promotion or support of fluoride use, including slow-release fluoride for treatment of osteoporosis (known to produce abnormal bone of inferior strength), these responses, although disappointing, are perhaps not too surprising. But, in such an important matter, should not at least some balance of viewpoint have been represented? As seen in the videotape (a copy of which has been sent to the Academy) the attitude of some of the presenters and panelists toward those who cited contrary data and questioned why such findings were not discussed can only be described as condescending and demeaning.

Today, with so many additional sources of fluoride present in processed foods, commercial beverages, and dental care products that were not there when water fluoridation began, the total intake of fluoride, even among children, has increased to as much as 2-5 milligrams or more per day, well above the initially proposed optimum of 1 mg/day (from one liter of 1-ppm fluoridated water). With these higher levels of fluoride intake, dental fluorosis and other toxic effects noted above have also increased.

We are sure that you would agree that it is immensely important to both the national interest and the world of science that the publications of the National Academy of Sciences maintain the highest standards of competence, objectivity, and integrity. In our view, unless the section on fluoride is withdrawn from this report on essential nutrients it could seriously threaten those standards. Therefore, we urge you to remove this section, and further request that should the fluoride issue be revisited by the Academy at some time in the future, that you should ensure that the investigating panel includes independent scientists who are fully conversant with the literature on the full range of fluoride's harmful effects.

Sincerely yours,

ALBERT W. BURGSTAHLER, Ph.D. (Organic Chemistry and Environmental Fluoride), Professor of Chemistry, The University of Kansas*, Department of Chemistry, 4035 Malott Hall, Lawrence, Kansas 66045.

ROBERT J. CARTON, Ph.D. (Environmental Sciences and Risk Assessment), Former Risk Assessment Manager for the Office of Toxic Substances, U.S. Environmental Protection Agency. Mailing address: 2455 Ballenger Creek Pike, Adamstown, MD 21710.

PAUL CONNETT, Ph.D. (Environmental Chemistry and Toxicology), Professor of Chemistry, St. Lawrence University*, Department of Chemistry, Canton, New York 13617.

RICHARD FOULKES, B.A.,M.D. (Physician). Former Consultant to the Minister of Health, Province of British Columbia, Canada. PO Box 278, Abbotsford, B.C., Canada V2S 4N9.

J. WILLIAM HIRZY, Ph.D., (Chemistry and Risk Assessment). Senior Vice President, National Federation of Federal Employees*, Local 2050, P.O. Box 76082, Washington D.C. 20013.

ROBERT L. ISAACSON, Ph.D., (Neurobehavioral Science). Distinguished Professor, Department of Psychology, Binghamton University*, Binghamton, NY 13902-6000.

DAVID C. KENNEDY, D.D.S., (Dentist). Past President of the International Academy of Oral Medicine and Toxicology*, 3243 Madrid Street, San Diego, CA 92110.

HAROLD D. KLETSCHKA, M.D., F.A.C.S., (Cardiovascular Surgeon). Past military consultant in thoracic and cardiovascular surgery to the U.S. Air Force Surgeon General and the Surgeon of Headquarters Command, Washington, D.C. Founder and first Chief of the USAF Cardiovascular Research Center (Parks Air Force Base, CA). Former Chairman, President and CEO of Bio-Medicus, Inc. Mailing address: 1925 Noble Drive, Minneapolis, MN 55422-4158.

LENNART KROOK, D.V.M., Ph.D., (Pathology). Cornell University*, Emeritus Professor of Pathology, New York State College of Veterinary Medicine, Ithaca, N.Y. 14853-6401.

RICHARD A. KUNIN, M.D., President, Society for Orthomolecular Health Medicine, 2698 Pacific, San Francisco, CA 94115

JOHN R. LEE, M.D. (Physician), 9620 Bodega Highway, Sebastopol, CA 95472.

WILLIAM MARCUS, Ph.D., (Toxicology).

GENE W. MILLER, Ph.D., (Biochemistry and Toxicology). Former Head of Biology, Associate I Dean of Science and Dean of Environmental Science, Utah State University*, Emeritus, College of Science, Department of Biology, Logan, Utah 84322-5305.

PHYLLIS MULLENIX, Ph.D. (Pharmacology and Neurotoxicology). Former Head of the Department of Toxicology, Forsyth Dental Center*, Boston. Research Associate, Department of Psychiatry, Children's Hospital*, Boston. Mailing address: P.O. Box753, Andover, MA 0180.

ALBERT SCHATZ, Ph.D. Microbiology). Former Professor of Science Education, Temple University*, Philadelphia, PA.

*These affiliations are listed for identification purposes only and do not imply endorsement of this letter by the institutions involved.

Sixteen weeks later the following letter was sent, also receiving
no reply or acknowledgment. Fluoride 1998;31(3):153-157

February 4, 1998

Kenneth I. Shine, M.D.
President, Institute of Medicine
National Academy of Sciences
2101 Constitution Ave. NW
Washington, DC 20418

Dear Dr. Shine:

Last October my co-signers and I sent to Dr. Bruce Alberts the enclosed joint letter concerning the fluoride recommendations in the impending publication by the National Academy Press of the report on Dietary Reference Intakes for Calcium, Phosphorus, Magnesium, Vitamin D, and Fluoride. Although we do not understand why we have not received a reply, we trust that our letter was brought to the attention of the Food and Nutrition Board of the Institute of Medicine for appropriate action.

When we submitted our letter we were under the impression that the position of the Food and Nutrition Board on the questions we raised was not yet settled. We have since learned, however, through the publication of the full text of the Summary of the report in the September/ October 1997 issue of Nutrition Today, pp. 182-188, that the upper level intake and other recommendations for fluoride had already been officially submitted for general distribution, even at the time the September 23rd workshop on the report was held at the Academy.

Does the appearance of the pre-publication version of the report Summary in that issue of Nutrition Today (which only reached our science library here on November 13) mean that the Food and Nutrition Board still considers an intake of 10 milligrams of fluoride per day (Table S-6) to be a tolerable upper level for persons over age 9 without significant risk of serious adverse health effects?

What is especially troublesome about the Board's position on this matter is that it explicitly and emphatically contradicts the recently published views of the most distinguished and long-time fluoride expert member of the Panel on Calcium and Related Nutrients - Professor Gary M. Whitford of the Medical College of Georgia. In the second, revised edition of his widely-cited monograph on The Metabolism and Toxicity of Fluoride (Karger, Basel, 1996), he states on page 138 (copy enclosed):

"Most estimates indicate that crippling skeletal fluorosis occurs when 10-20 mg of fluoride have been ingested on a daily basis for at least 10 years." With this clinical condition, he notes, "... bone ash fluoride concentrations generally exceed 9,000 ppm. Calcification of ligaments often precludes joint mobility and numerous exostoses may be present. These effects may be associated with muscle wasting and neurological complications due to spinal cord compression."

Why do the recommendations of the Food and Nutrition Board on this critical matter contradict these well-considered views of the leading fluoride expert on the Board's Panel on Calcium and Related Nutrients? Clearly, a fluoride intake level that produces "crippling skeletal fluorosis" can hardly be regarded as tolerable and certainly should not remain uncorrected.

Although it is widely believed that "... crippling skeletal fluorosis has not been and is not a public health problem in the USA" (Whitford, op. cit., page 137), the same cannot be said of the situation in other parts of the world, e.g., in China, India, the Middle East, and Africa, where crippling skeletal fluorosis is still a serious endemic health problem—even at less than 10 mg/day fluoride intake. Moreover, in the absence of sufficient numbers of contemporary biopsy and necropsy bone fluoride analyses, it is very unwise to assume that little or none of the extensive middle and old-age osteoarthritis that plagues so many people in the United States is not an undiagnosed manifestation of various stages of skeletal fluorosis.

In this connection it is important to note that otherwise unexplained intermittent episodes of gastric pain and muscular weakness have been clinically linked in areas of endemic dental and skeletal fluorosis to fluoride intakes as low as 2 to 5 mg/day (ref. 1). These peer-reviewed reports fully validate earlier clinical findings of the occurrence of these very same and related effects in fluoridated communities in the United States and other countries which have been discounted or ignored without scientific refutation (ref. 2).

Today, when many officials at all levels in our government seem to have difficulty in being forthright and admitting what is true, it ill behooves us as scientists not to tell the public what is known to be true, whether or not it agrees with what is generally accepted as true. "For truth is truth, though never so old, and time cannot make that false which was once true." (ref. 3).

Because the recommendations of your report on Dietary Reference Intakes for Calcium, Phosphorus, Magnesium, Vitamin D, and Fluoride have been released to the public before correction of the serious errors and oversights pointed out here and in previous communications to the Food and Nutrition Board, I presume there is no objection to this letter being made part of the public record.

Yours sincerely,

Albert W. Burgstahler, Ph.D.
Professor of Chemistry

Enclosures:  Copy of October 15, 1997 letter to Dr. Bruce Alberts
     Page 138 of the 2nd, revised edition of The Metabolism and Toxicity of Fluoride

Copy: Bruce Alberts
    Gary M. Whitford
    Co-signers of October 15, 1997 letter to Dr. Alberts


  1. A.K. Susheela et al. Fluoride Ingestion and its Correlation with Gastrointestinal Discomfort. Fluoride 25:5-22, 1992; Prevalence of Endemic Fluorosis with Gastrointestinal Manifestations in People Living in Some North-Indian Villages. Fluoride 26:97-104, 1993; S. Desarathy et al. Gastroduodenal Manifestations in Patients with Skeletal Fluorosis. Journal of Gastroenterology 32:333-337, 1996.
  2. G.L. Waldbott. Incipient Fluorine Intoxication from Drinking Water. Acta Medica Scandinavica 156:157-168, 1956; Fluoride in Clinical Medicine. Supplement 1 to International Archives of Allergy and Applied Immunology 20:1-60, 1962; Fluoridation: A Clinician's Experience. Southern Medical Journal 73:302-306, 1980; 74:519, 1981.
  3. Letter of Edward de Vere, 17th Earl of Oxford, May 7, 1603. Cf. William Shakespeare. Measure for Measure, V.1.45-46:
    ". . . for truth is truth To the end of reckoning."

Discussion Section: Fluoride 1999;32(3):187-198
EDITOR’S NOTE [Professor Albert Burgstahler]

The two letters referred to at the beginning of the letter below were published in Fluoride 31(3) 153-157 August 1998.

In a separate letter from the National Academy of Sciences (NAS), also dated November 20, 1998, James Jensen, Director of the National Research Council Office of Congressional and Governmental Affairs of NAS, replied to an inquiry from Pennsylvania Senator Arlen Specter on behalf of one of his constituents, who wanted to know why my joint letter of October 15, 1997 to Dr. Bruce Alberts, President of NAS, had not received a reply. In his letter to Senator Specter, Mr. Jensen wrote:

"When Dr. Burgstahler’s letter on fluoridation [actually, it was about the proposed Dietary Reference Intake standards for fluoride and only indirectly about fluoridation] arrived at the Academy, a response was drafted but never sent out. There is little excuse for this, but this is what occurred. . . .

"Please accept our sincere apologies. There was no intent to show disrespect to your constituent."

The letter below, therefore, although "drafted" earlier, was sent only after prompting from Senator Specter’s inquiry.


2101 Constitution Avenue, Washington, D.C. 20418

November 20, 1998

Albert W. Burgstahler, Ph.D. and others
Professor of Chemistry
The University of Kansas
4035 Malott Hall
Lawrence, Kansas 66045

Dear Dr. Burgstahler:

We apologize for the delay in responding to your letters of October 15, 1997 and February 4, 1998, to each of us individually. At the time we had a very large number of inquiries and comments, and while letters were prepared in response to your letter along with the others, for some reason they did not reach you. The letter that we found in our files is reprinted below.

We want to thank you and your co-signers for your October 15, 1997 letter to us concerning the Food and Nutrition Board’s (FNB) recent report, Dietary Reference Intakes for Calcium, Phosphorus, Magnesium, Vitamin D and Fluoride. The publication of the report represents the initial report of a major new activity of the FNB: the development of a comprehensive set of reference values for nutrients and food components of possible benefit to health, that may not meet the traditional concept of a nutrient. If adequate scientific data exist that support a health benefit from the inclusion of these components in the diet, reference intakes will be established.

In replying to your letter, we have consulted with the Committee that produced the FNB report and asked them to review the important points that you raised concerning their report and the associated workshop, as well as to explain why they have reached the conclusions they reached despite the information you cite.

First, let us reassure you with regard to one concern. Nowhere in the report is it stated that fluoride is an essential nutrient. If any speaker or panel member at the September 23rd workshop referred to fluoride as such, they misspoke. As was stated in Recommended Dietary Allowances 10th Edition, which we published in 1989: "These contradictory results do not justify a classification of fluoride as an essential element, according to accepted standards. Nonetheless, because of its valuable effects on dental health, fluoride is a beneficial element for humans." Dr. Vernon Young, Chair of the Standing Committee on the Scientific Evaluation of Dietary Reference Intakes, stated this at the workshop’s conclusion.

The adequate intake (AI) of fluoride for infants 0 to 6 months of age is set at 0.01 mg/day. As explained in Chapter I of the report, the average intake of a particular nutrient by full-term infants who are born to well-nourished mothers and exclusively fed human milk has been adopted as the basis for deriving an AI for all nutrients and other food components during the first 6 months of life. Using the human milk-fed infant as the model supports the recommendation that exclusive breast feeding is the preferred method of feeding for normal full term infants for the first 4 to 6 months of life - a recommendation shared by the Canadian Paediatric Society (Health Canada, 1990), the American Academy of Pediatrics (1982), and the Food and Nutrition Board’s report Nutrition During Lactation (IOM, 1991). (Infants who are exclusively breast fed for the first six months of life would have a low fluoride intake, and yet scientific evidence showing that these infants are at greater risk for dental caries than formula-fed infants is lacking.) During the second six months of life and thereafter, the AI for fluoride from all sources is set at 0.05 mg/kg/day because it confers a high level of protection against dental caries and is associated with no known unwanted health effects.

Although the report acknowledges that most of the anti-caries effect attributed to fluoride occurs by topical exposure, it does not matter whether that exposure is from food, water or dental products. As you state, the prevalence of caries in some countries around the world without water fluoridation has declined over the years. This has been attributed to national dental hygiene programs and the use of fluoride in school-based prevention programs (rinses or tablets), as well as to the use of fluoridated toothpaste. These programs provide both systemic and topical fluoride exposures.

In following the model for the development of Tolerable Upper Intake Levels (ULs), as explained in Chapter 3 of the report, moderate enamel fluorosis was considered as the critical adverse effect in children under 9 years of age. As noted by Dean and coworkers some 60 years ago, mild enamel fluorosis was present in some residents of areas where water contained < 2 mg/liter of fluoride. At that time the diet, particularly the water, was the only significant source of fluoride so that the daily intake of fluoride could be estimated with reasonable accuracy. The average intake by children at risk was 0.05 mg/kg/day. The prevalences of both dental caries and fluorosis in these communities was low and there is no reason to expect that level of intake (from all sources) to produce different results today. Compared with Dean’s findings, recent studies have revealed a higher prevalence of dental fluorosis in the United States and Canada, including a few cases of moderate fluorosis. However, analytical epidemiological studies have repeatedly shown that the major risk factors are ingestion due to the early use of fluoride toothpaste and/or the use of dietary supplements. Thus, the total fluoride intake by some children whose water is fluoridated is now higher than in Dean’s time. This is the reason that age-specific intakes for total fluoride, including that from dental products, are based on 0.05 mg/kg/day. To the extent that this intake level is followed, the prevalence of dental fluorosis can be expected to decline while a healthy dentition is maintained.

Three recent reviews of the literature, Kaminsky et al., 1990; NRC, 1993; USPHS, 1991, attempted to identify adverse functional effects of fluoride ingestion in adults. Fluoride exposures included those associated with drinking water containing as much as 8 mg/liter of fluoride and the use of dental products. These reviews concluded that evidence linking chronic, high fluoride exposures with adverse effects such as cancer, including osteosarcoma, birth defects, genetic disorders, or bone fractures is either insufficient or highly contradictory. In addition, the majority of animal studies have shown no effect on cancer, birth defects, genetic disorders or bone strength of very high and long-term fluoride exposures [FFO-OLF comment: this was then, and remains even today, totally false]. Thus, the primary adverse effects associated with chronic, excess fluoride intake are enamel fluorosis in children through 8 years of age and skeletal fluorosis in adolescents and adults over 8 years of age. In Hodge's 1979 article, he reported that evidence of crippling fluorosis "was not seen in communities in the United States where water supplies contained up to 20 ppm." [FFO-OLF comment: We now know that this report was falsified, and proven so in a court of law] In such communities daily fluoride intakes of 20 mg would not be uncommon.

Fluoride is continuously taken up by newly formed bone and released from older bone being resorbed. As long as intake remains constant, the concentration in bone tends to increase during life. It is not entirely clear why this happens but it may be due to the preferential resorption of bone crystallites that do not contain fluoride. In any event, in the United States and Canada, it is known that the development of skeletal fluorosis, even in earliest stages, has not occurred, even where the water fluoride concentrations have been in excess of 10 ppm [FFO-OLF comment: once again, a total falsehood, a fabrication].

In reviewing Kaj Roholm’s classic 1937 report of bone changes among Danish cryolite workers, it was noted that Roholm reported no intake data for fluoride, apparently because the researchers were not able to measure air-borne fluoride. On page 279, Roholm states: "It must be admitted that with respect to the important question of dose, that the observations available are sporadic and to some extent contradictory; in most of the spontaneous intoxications the intake (his word) quantity of fluoride is not known at all."[FFO-OLF comment: another falsehood] Later on page 319 Roholm states: "In man the disease (he is referring to crippling skeletal fluorosis) is probably caused by 0.20-0.35 mg fluoride daily per kg body weight." The reason for this estimate is not given. It is unfortunate that, in the absence of scientific data, these estimates were ever made. Although we are uncertain about the lower level of intake and time of exposure that causes clinically significant skeletal fluorosis, we do know that, at least for U.S. and Canadian citizens, intakes associated with water fluoride concentrations in excess of 10 ppm do not cause clinically significant skeletal fluorosis[FFO-OLF comment: another falsehood].

Our study was funded entirely by the governments of the United States and Canada. The funding agencies were the National Institute of Health’s National Heart, Lung, and Blood Institute; the Agricultural Research Services of the U.S. Department of Agriculture; U.S. Food and Drug Administration; and Health Canada.

We thank you and your co-signers for your careful reading of the report and interest in assuring its accuracy and completeness. Given the complexities of the issues the report considers, we are confident that much room remains for further objective inquiry. We have tried to give you some of the reasons for the Committee’s conclusions. However, we hope that the report will lead to additional research on which to base dietary reference intakes - for both essential nutrients and other dietary constituents with documented health benefits.

Once again, we regret that this reply to your thoughtful letter did not reach you much earlier, when it was prepared.


Bruce Alberts, Ph.D.
National Academy of Sciences

Kenneth Shine
Institute of Medicine

National Academy of Sciences fails to respond again!
EDITOR’S COMMENT [published in Fluoride 1999:32(3);191-192]

On January 12, 1999, the following letter was faxed to Drs. Alberts and Shine:

Drs Bruce Alberts and Kenneth Shine
National Academy of Sciences & Institute of Medicine
2101 Constitution Avenue NW
Washington, DC 20418

Fax: (202) 334-2316

Dear Drs. Alberts and Shine,

Your letter of November 20, 1998 in response to my letters of October 15, 1997, and February 4, 1998, awaited me on my return late last month from an extended trip to the Far East beginning in mid-November. A related letter dated November 19, 1998, from Professor Gary M. Whitford had also arrived.

Next week I plan to attend the workshop scheduled for January 21 at the Academy. Several others who cosigned my October 15, 1997, letter also plan to be there.

In view of the gravity of the issues addressed in these letters, would it be possible for some of us to meet briefly with either or both of you before 11:00 a.m. on Wednesday, January 20, at the National Academy of Sciences?

I will be leaving Lawrence early Monday morning (January 18), so the favor of your early reply by fax or e-mail (addresses below) would be appreciated.

Yours sincerely,

Albert W. Burgstahler
Professor Emeritus of Chemistry
The University of Kansas

There was no reply to the above letter. Upon my arrival at the NAS headquarters in Washington on the morning of January 20, there was still no reply, and no meeting could be arranged with either Dr. Alberts or Dr. Shine.

As indicated at the end of my February 4, 1998 letter to Dr. Shine (see Fluoride 31(3) 157 August 1998), I also sent a copy of that letter to Professor Gary M. Whitford of the Medical College of Georgia, who was the ranking fluoride expert on the review panel. Then on February 17, 1998, I again wrote to Professor Whitford, specifically asking why his views, published prominently in the 1996 edition of his monograph, Metabolism and Toxicity of Fluoride (p. 138), that "crippling skeletal fluorosis occurs when 10-20 mg of fluoride have been ingested on a daily basis for at least 10 years," were set aside in favor of suggesting that a much higher level of fluoride intake is required to produce this effect.

Nine months later a reply finally arrived from Professor Whitford. Dated November 19, 1998, just one day before the date on the foregoing letter from Drs. Alberts and Shine, Professor Whitford stated in his letter: "During the course of assisting with the development of the DRIs [Dietary Reference Intakes],…I concluded that the literature does not support the likelihood [sic] of advanced skeletal fluorosis in U.S. residents whose daily intake does not exceed 10 mg." This statement, however, is contradicted by the evidence presented in my letter of February 4 to Dr. Shine.

It is also of interest that much of the material in Professor Whitford’s letter to me is found in the November 20, 1998 letter from Drs. Alberts and Shine, including the passage from Roholm’s treatise Fluorine Intoxication – A Clinical Hygienic Study, that a daily fluoride intake of 0.20-0.35 mg/kg body weight is likely to cause crippling skeletal fluorosis. But then Drs. Alberts and Shine go on and boldly assert: "…we do know that, at least for U.S. and Canadian citizens, intakes associated with water fluoride concentrations in excess of 10 ppm fluoride do not cause clinically significant skeletal fluorosis."

But clearly, the average fluoride intake of an adult drinking water containing more than 10 ppm fluoride will very likely exceed 10 mg/day and therefore, according to Professor Whitford, would create a risk for crippling skeletal fluorosis, even in the United States and Canada. Why residents of these two countries supposedly do not develop skeletal fluorosis from levels of fluoride intake that are well known to cause it elsewhere is deftly shoved aside by citing studies in the U.S. that did not report finding it.

Equally disturbing in the Alberts-Shine letter is the unexplained jump of an "adequate" fluoride intake of only 0.01 mg/day for infants up to age six months to 0.05 mg/kg body weight/day for the second six months of life and thereafter. By age six months, a baby weighing 6-8 kg would therefore have an "adequate" fluoride intake of 0.3 to 0.4 mg/day  –  a 30- to 40-fold increase from the first six months to the second six months of life after birth! No such huge increase is proposed for any other dietary component.

As pointed out by Dr. John Yiamouyiannis at the end of the following letter, this 0.05 mg/kg/day figure for fluoride appears to be based on an effort to justify or "sanctify" water fluoridation. Thus, an average daily total fluoride intake of 3.5-mg by a 70-kg adult drinking 1-ppm fluoridated water amounts to 3.5 mg/70 kg/day or 0.05 mg/kg/day. And this is sound "scientific" thinking by the U.S. National Academy of Sciences?

In the end, however, all these considerations are moot, since the basis for setting an "adequate intake" of fluoride rests on its alleged ability to prevent tooth decay. But since any such dental benefit from fluoride, to whatever extent it exists, is now known to be largely topical and not systemic (from ingestion), how can there even be a daily "adequate intake"? [FFO-OLF comment: however, it must now be acknowledged that even this type of use of fluoridated substances is a seriously questionable practice, in light of recent investigations and research on the effects of fluoride on teeth, bodily calcium and other human biological substances. See Bruce Alberts, PhD, letter below.]

Discussion Section continued Fluoride, 1999;32(3):193-198

Safe Water Foundation
6439 Taggart Road, Delaware, Ohio 43015

Bruce Alberts, Ph.D.
President, National Academy of Sciences
Kenneth Shine, M.D.
President, Institute of Medicine
2101 Constitution Avenue NW
Washington, DC 20418

Dear Drs. Alberts and Shine:

A copy of your November 20, 1998 letter to Professor Albert Burgstahler has been sent to me for comment. If you actually believe what you wrote in that letter, I am sure you will welcome the following information.

I. In your letter, you cite the 10th edition of Recommended Dietary Allowances as stating that while fluoride cannot be classified as an essential element, [but] "because of its valuable effect on dental health [which you later define as its ‘anticaries effect’], fluoride is a beneficial element for humans." You then state as a fact that the intake of .05 mg/kg/day of fluoride confers a high level of protection against dental caries. Implicit in your letter is the claim that fluoridation of water reduces tooth decay. You then explain that part of the reason for the decline in tooth decay in nonfluoridated areas is due to the administration of fluoride tablets.

However, as any informed professional would know, there is a general consensus among experts on both sides of the fluoride issue that swallowing fluoride does nothing to prevent tooth decay. In fact, the only proven effect that swallowing fluoride has on teeth is to poison ameloblasts and odontoblasts, resulting in dental fluorosis, the formation of imperfect or damaged enamel or dentine, respectively, and slowing down the eruption rate of deciduous teeth.

Evidence that swallowing fluoride does not prevent tooth decay

- In water

All the recent large-scale studies taken together show that fluoridation is ineffective in reducing the decay rate of permanent teeth.

Earlier studies claiming a reduction in tooth decay have already been discredited by those who have and/or still do promote fluoridation. For example, Dr. John Colquhoun, former Chief Dental Officer of Auckland, New Zealand and at one time the President of the Fluoridation Society conducted the largest tooth decay study and found no difference in tooth decay rates in fluoridated and nonfluoridated areas in New Zealand. Dr. A.S. Gray, former Chief Dental Officer of British Columbia, found that British Columbia, the province with the lowest fluoridation rate in Canada, also had the lowest tooth decay rate in Canada. And Dr. Elmer Green and Taimi Carnahan, two of the most ardent promoters of fluoridation, coauthored a study with two others that showed that there was no significant difference in the tooth decay rates in fluoridated Newburgh and nonfluoridated Kingston (in 1986) despite the fact that these two cities were used to show that fluoridation reduced tooth decay rate by 70% (from 1945 to 1955) {J.V. Kumar, et al., "Trends in Dental Fluorosis and Dental Caries Prevalences in Newburgh and Kingston, NY", American Journal of Public Health, Volume 79, pp. 565-569 (1989)}.

Even Dr. Hardy Limeback, the fluoride expert for the Canadian Dental Association admits that the ingestion of fluoride does nothing to reduce tooth decay. On February 14, 1998, he wrote:

You should be glad to know that I no longer take such a profluoride stand. I don't care if I alienate all my dental public health colleagues anymore on this whole issue and I realize just how much out on a limb I'm climbing in no longer supporting water fluoridation.

Putting hydrofluorosilicic acid from smoke stack scrubbers to fluoridate the water for me was the breaking point.

Consider me still a pro-fluoride dentist but a converted antifluoridationist who now advocates that we stop putting toxic waste in Canadian water supplies shame!

- In tablet or drop form

Contrary to your claims, fluoride tablets have been shown to be ineffective in reducing tooth decay in the Rand report sponsored by the Robert Wood Johnson Foundation (Robert Wood Johnson Foundation Special Report No.2, 1983) and in the scientific literature {H Kalsbeek, et al., Use of fluoride tablets and effect on prevalence of dental caries and dental fluorosis, Comm Dent Oral Epidemiol 20:243-245 (1992)}.

II. In your letter, you claim that part of the reason for the decline in tooth decay in nonfluoridated areas is due to the use of fluoride in school-based rinse programs.

Contradicting this unsubstantiated claim, a Rand Corporation study {Disney, et al., A case study in contesting the conventional wisdom. school-based mouthrinse programs in the USA, Comm Dent Oral Epidemiol 18:46-56 (1990)} has shown that topical fluoride exposure in school programs does not reduce tooth decay rates.

III. You acknowledge that "recent studies have revealed a higher prevalence of dental fluorosis" and claim that this is "due to the early use of fluoride toothpaste and/or the use of dietary supplements."

The absurdity of this can be seen by comparing the 1-2 mg per day children get from fluoridated water with the 1/4 mg per day of fluoride these same children get from ingesting toothpaste. While there are many studies showing the fluoridated water causes dental fluorosis, there are no studies showing that fluoride ingestion from fluoridated toothpaste by itself causes dental fluorosis. [This is not to deny, however, that the approximate 1/4 mg/day of fluoride consumed from toothpaste might push the total fluoride intake over the top to cause dental fluorosis in marginal cases].

The fact that fluoridation causes dental fluorosis is obvious from your own NRC, 1993 report. Let’s ask it some questions:

Does fluoridation result in dental fluorosis (fluoride-induced tooth damage)?

According to page 37 of your report: "...the prevalence of dental fluorosis in optimally fluoridated areas (both natural and added) in recent years ranged from 8% to 51%, compared with 3% to 26% in nonfluoridated areas."

Two things are obvious here: (1) we can safely assume that fluoride toothpaste usage is similar in both fluoridated and nonfluoridated areas and (2) we know that fluoride supplement use is higher in nonfluoridated areas – yet dental fluorosis rates are twice as high in fluoridated areas.

As a result, should we stop water fluoridation?

According to page 43 of your report: "Indeed, most dental researchers (Horowitz, 1991; Rozier, 1991 Szpunar and Burt, 1992) believe that the best approach to stabilizing the prevalence and severity of dental fluorosis is to control fluoride ingestion from foods, processed beverages, and dental products rather than reduce the recommended concentrations of fluoride in drinking water."

And on page 44 of your report it is stated: "Fluoride in foods and beverages processed with fluoridated water has long been suspected as a risk factor.…"

But how can you control fluoride ingestion from foods and beverages processed with fluoridated water?

According to page 48 of your report: "applying such a policy would be formidable; reductions of fluoride in drinking water would be easier to administer, monitor, and evaluate."

The mission to fanatically support water fluoridation has apparently allowed you to disregard any form of logic, if necessary, in the production of your NRC, 1993 report.

IV. In you[r] letter, you claim to rely on "Three recent reviews of the literature, Kaminsky, et al., 1990; NRC, 1993;, and USPHS, 1991."

Enclosed are critiques of Kaminsky, et al., 1990, NRC, 1993, and USPHS, 1991.

V. In your letter, you claim "the majority of animal studies have shown no effect on cancer, birth defects, genetic disorders, or bone strength".

I have enclosed a list of 10 animal studies that show that fluoride initiates tumors and/or cancer and/or promotes tumor growth rate and/or increases the cancer-causing potential of other carcinogens. Can you come up with 11 negative animal studies?

I have enclosed a list of 2 animal studies that show that fluoride has an effect on birth defects. Can you come up with 3 negative animal studies?

I have enclosed a list of 22 animal studies that show that fluoride causes genetic disorders. Can you come up with 23 negative animal studies? In your own publication, NRC, 1993, on Table 6-2, you list six in vitro animal studies, five of which deal with the effect of fluoride on genetic disorders (aberrations) and all five of which found that fluoride exposure caused chromosomal damage. In table 6-6, you list four in vivo studies which deal with the effect of fluoride on genetic disorders (aberrations), two of which are listed as showing positive results and two of which are listed as showing negative results.

While I don’t have a large number of animal studies regarding the adverse effects of fluoride on bone strength of very high and long-term fluoride exposures, I do have a large number of human clinical and epidemiological studies, for a total of 34 references. Can you provide 35 negative studies?

VI. At this point, it must be obvious how preposterous is the statement made in your letter: "Thus, the primary adverse effects associated with chronic excess fluoride intake are [moderate] enamel fluorosis in children through 8 years of age and [crippling] skeletal fluorosis in adolescents and adults over 8 years of age."

But this statement not only covers up the well-documented findings that fluoride causes and/or promotes tumors and cancers as well as possibly enhancing the cancer-causing effects of other carcinogens and that fluoride causes genetic damage down to and including the levels proposed in your "adequate intake" recommendations, it also claims that you can recommend safe upper levels where children and adults can suffer from dental and skeletal fluorosis so long as the damage does not reach the level of moderate or crippling. Borrowing a word from Dr. Limeback - "shame!"

To make matters worse, the upper level for fluoride suggested, i.e. 2.2 mg per day for children 4-8 years of age, does not preclude moderate-to-severe dental fluorosis. Your own publication, NRC, 1993, table 2-5 shows that about 5-10% of these children will suffer from moderate-to-severe dental fluorosis.

It is astounding that in your letter, you never indicate what skeletal fluorosis is. Skeletal fluorosis simply refers to changes in the bone or tissues associated with the bone that result from the poisoning of fibroblasts, chondroblasts, and osteoblasts by fluoride. One form of skeletal fluorosis is osteoporosis, which can manifest itself in the form of increased hip fracture rates; and, at levels of about 1 mg/l in the drinking water, an increase in hip fracture rates has been reported in no less than four papers (two articles and two letters) published in JAMA since 1990.

By disturbing the protein extruded by blastic cells, fluoride can trigger autoimmune responses leading to rheumatoid arthritis (which can be crippling but will not be detectable in x-rays) or induce the calcification of ligaments, tendons, and cartilage which will only be observable in x-rays in the later stages. Both osteosclerosis and osteoid seams can be triggered by fluoride. None of the outdated studies (1941, 1954, 1955, 1957) cited by Gary Whitford are capable of detecting skeletal fluorosis even if they had been done today, due to lack of a control group in one, lack in numbers in three, and exclusive use of x-rays in one. On pages 50-53 of my book, Fluoride, the Aging Factor, I describe documented cases of skeletal fluorosis occurring among people consuming water containing fluoride at levels of 0.7 mg/l to 9.4 mg/l.

Your Dietary Reference Intake values (DRIs) for calcium, phosphorus, magnesium, vitamin D, and fluoride are published in Nutrition Today, volume 32, pages 182-188. Looking at the mg/kg/day values of each of these substances relative to their 0-6 month value, each DRI goes down or stays the same after maturity, except for fluoride, which in contrast goes up about 3000%! Why? Just to sanctify fluoridation.


John Yiamouyiannis, Ph.D.

January 19, 1999


  1. See, for example, Yoshitsugu Imai, "Relation Between Fluoride Concentration in Drinking Water and Dental Caries in Japan", Koku Eisei Gakkai Zasshi, Volume 22, No. 2, pp. 144-196 (1972); R.M. Bell, et al., "Results of baseline dental exams in the national preventive dentistry demonstration program". R-2862-RWJ. Santa Monica, CA. Rand Corporation. 1982; J. Colquhoun, "Child Dental Health Differences in New Zealand", Community Health Studies, Volume 11, pp. 85-90 (1987). A.S. Gray, "Fluoridation: Time for a New Baseline?" Journal of the Canadian Dental Association, Volume 53, pp. 763-765 (1987); C.F. Hildebolt, et al., "Caries Prevalences among Geochemical Regions of Missouri", American Journal of Physical Anthropology, Volume 78, pp. 79-92, (1989); J.A. Yiamouyiannis "Water Fluoridation and Tooth Decay: Results from the 1986-1987 National Survey of U.S. Schoolchildren", Fluoride 1990; 23: 55-67.
  2. Although there is good evidence that the decay rate of deciduous teeth is lower among 5-year-olds in fluoridated areas, this reduced tooth decay rate rapidly disappears among 6- and 7-year-olds and is no longer apparent in 8-year-olds. This temporary reduction may be due to the inhibitory effect of fluoride on tooth eruption which has already been reported (see for example S. S. Krylov and K. Pemrolyd, "Deciduous tooth eruption and fluorosis in the case of increased fluorine content in the drinking water", Stomatologiia, (Mosk) Volume 61, pp. 75-77 (1982)). In any event, there is no reason to believe that the intake of fluoride beyond the age of five would have any effect on the tooth decay rate.
  3. I assume that you are referring to original studies (not reviews) that looked into these matters and are not just playing word games. It is obvious that there are hundreds of thousands of animal studies that have not found that fluoride causes e.g. genetic damage because there are hundreds of thousands of animal studies that have not looked at genetic damage and hundreds of thousands of animal studies that have not looked at fluoride. I mention this only because when the National Cancer Institute was asked, during Congressional Hearings on fluoride and cancer in 1977, to produce studies showing that fluoride did not cause cancer, 11 of the 13 references they produced did not even deal with fluoride and cancer.
  4. One of the two studies you claim shows negative results is Voroshilin, 1975, which is an apparent translation of his original paper in 1973, which I had translated. But even in the 1973 paper, the original English summary points out: "An increase from 1.24 (in the control) to 6.5% in the frequency of cells with structural chromosomal aberrations was observed in the bone marrow of albino rats after 5 months treatment with cryolite [at a 3.0 mg/m3 concentration. After a mixture of 0.5 mg/m3 of cryolite and 0.5 mg/m3 of hydrogen fluoride for five months, the increase was from 1.24 (in the control) to 5.9%. For comments on the second paper by Martin, 1979, see the footnote on page 66 of my book, Fluoride, the Aging Factor (enclosed).
  5. C.A. Jones, et al., "Sodium fluoride promotes morphological transformation of Syrian hamster embryo cells", Carcinogenesis, Volume 9, pp. 2279-2284 (1988) and supported by the findings of R.N. Muhkerjee and F.H. Sobels, The effect of fluoride and iodoacetamide on mutation by X-irradiation in mature Spermatazoa of Drosophila, Mutation Research, volume 6, 217-225 (1968).
  6. not to mention secondary effects on bone that fluoride may have through its effects on the parathyroid.
  7. Please explain to me what you mean in your final conclusion "...intakes associated with water fluoride concentrations in excess of 10 ppm do not cause clinically significant skeletal fluorosis."

NOTE: The foregoing letter has not received a reply or even an acknowledgement.


DIETARY REFERENCE INTAKES Calcium, Phosphorus, Magnesium, Vitamin D, and Fluoride
(Institute of Medicine, National Academy of Science, Washington DC 1997)

Reviewed by Richard G Foulkes BA MD, Fluoride, 1997, 30:4

This report, "Dietary Reference Intakes", in the words of its Preface "represents the initial report of a major new activity of the Food and Nutrition Board (FNB): the development of a comprehensive set of reference values for dietary nutrient intakes for the healthy population in the United States and Canada." A new activity that may refer to fluoride is "the examination of data about selected food components that have not been considered essential nutrients" (p vii).

With regard to fluoride, anyone familiar with previous US government reports on this subject (1,2) cannot avoid the conclusion that the report under review has as its objective the justification (or rationalization) of present high intake levels of fluoride by every age group, including pregnant and lactating females, that have been forced upon all by government policy. The report presents no new research to prove once and for all time in a way that can be replicated that fluoride (fluorine} is a nutrient that is "essential" for human growth and development. Neither the Food and Drug Administration (FDA) in 1978, nor the National Research Council/National Academy of Sciences {NRC/NAS) in 1989, has accepted the view that fluoride is an essential nutrient biologically for man.

This report is a review of selected references and contains errors, omissions, contradictions and biased manipulations of information. An adequate critique would have to be on a paragraph by paragraph basis thereby leading to the production of a lengthy volume. This would take resources not available to those whose cause is not favoured, as is the report under review, by the public purse.

It is not surprising to note that Health Canada is one of the contributors. A report prepared for Health Canada by a group of Canadian pro-fluoridation dental academicians was published in July 1994. (3) This effort resembles the present report in many ways. It was, in my view, an example of "tainted truth". (4)

To be specific: Does the Dietary Reference Intakes report present solid replicable evidence that fluoride is a nutrient to be placed alongside calcium, phosphorus, magnesium and vitamin D as a biochemically essential component of the human diet? Such positive evidence is a sine qua non. Without it, the proposals for a Recommended Daily Allowance (RDA), Estimated Average Requirement (EAR), Adequate Intake (AI), and Tolerable Upper Intake Level (UL) are without meaning. The UL, however, may be significant in estimating the possibilities of incurring adverse effects of fluoride which may be classified as a ubiquitous inessential component or a contaminant of the diet.

The report makes it clear (p 2 9) that "evidence on which to base an actual requirement (for fluoride) is scant ... Because data are not available to determine an Estimated Average Requirement (EAR), the reference value that will be used for fluoride is the Adequate Intake (AI). The AI is based on estimated intakes that have been shown to reduce the occurrence of dental caries maximally in a population without causing unwanted side effects, including moderate fluorosis." (p 8-10).

To support this approach, the report presents the often used statement: "(the) ability (of fluoride) to inhibit and even reverse the initiation and progression of dental caries is well known. It also has the unique ability to stimulate new bone formation and, as such, it has been used as an experimental drug for the treatment of osteoporosis." (p 8 1)

As was the case in the Health Canada Report, no contemporary study could be found that effectively supports the belief in the cariostatic role. As a consequence, both reports are forced to present Dean's highly selective 1942 studies (and graphical representation) as the chief support. The authors of the Health Canada Report admitted that the 1986-87 survey of 39,000 plus US school children by the US National Institute for Dental Research (NIDR) was the most extensive contemporary study but showed no statistically significant difference between fluoridated and non fluoridated groups.

The report under examination makes no such concession. Its authors stress the insignificant "18%" (sic) difference reported by Brunelle and Carlos (5) and manipulate the data in the Regional Survey Results (6) to obscure the finding that when the least fluoridated region (Region VII, "Pacific") was compared to the most highly fluoridated region (Region III, "Midwest") the least fluoridated population had the most children who were caries-free. The report fails to cite similar findings from Canada (Gray 1987)7 and New Zealand (Colquhoun 1993) (8).

The authors of the report also deal with the effects which occur at very low intake of fluoride which they term "negative balance". They are forced to admit (p 8 10) that "no data document the effects of long term negative balance on enamel, on salivary or plaque concentration or on caries development."

The "evidence" for the cariostatic activity of fluoride consists of the presentation of questionable data from the 1940s and of the manipulation of the results of contemporary surveys. There are no data that show detrimental effects of long-term absence of dietary fluoride. For these reasons, fluoride cannot be considered a nutrient along with such dietary components as calcium and vitamin D for which substances evidence is clear with regard to both positive contribution to health and negative physiological effects of long term absence.

On the basis of their belief in the cariostatic action of fluoride, the authors of this report tabulate (Table S 5, p S 11) the "criteria and dietary reference intake values for fluoride by "life stage group". The Adequate Intake (AI) for fluoride ranges from 0.01 mg/day for both sexes 0 6 months through 3.8 mg/day for males and 3.1 for females 19 to 70+ years. This includes 2.9 - 3.1 mg/day for both pregnant and lactating females. It is impossible to see these levels as "adequate" for anything but intoxication (poisoning) at some early stage for many individuals.

Of importance is the selective way in which the authors of this report derive the "Tolerable Upper Intake Levels (UL) by life stage group" presented in Table S 6 (p S 12). The report states that these values are "set to protect the most sensitive individuals in the healthy general population (such as elderly individuals who tend to have a decreased glomerular filtration rate)" (p S-11). The values range from 0.7 mg/day for 0 6 months to 10 mg/day for ages 9 years to 70 years, including pregnant and lactating females. There is contrary evidence even from sources cited by the authors, e.g. Hodge (1979),9 who states that 10 25 mg/day over a period of 10-20 years can produce crippling skeletal fluorosis.

Important omissions are frequent in the selected studies used to produce these estimates. Enamel fluorosis is termed an "adverse cosmetic effect" rather than a "functional adverse effect", even in its most advanced forms (p 8 15). The authors refer to the papers by Fejerskov where his statements can be used to support their bias. They omit his description of the severity of the structural damage found in dental fluorosis (10) and his comment that "a daily dose of fluoride as low as 0.04 mg/kg body weight can result in dental fluorosis of the permanent dentition" (10) - presumably because they have selected an "optimal" daily level of 0.05 mg/kg body weight which, by comparison, is too high. They also ignore Fejerskov's comment that "a magic borderline below which the signs of dental fluorosis are totally absent for all people does not in reality exist." (11)

The report presents a case for increased bone density caused by fluoride but fails to discuss, in a meaningful way, the quality of bone produced and to take seriously the complicating factor of increased fracture of the femur (hip). With regard to the latter, the report plays down the effect on hip fractures of residence in fluoridated areas. Lee (12) points out that this relationship was shown to be positive in 7 out of 10 recent surveys comparing incidence relative to fluoridation status (including the results of two workshops held under the auspices of the NAS). In the same paper, Lee shows how the three negative studies deserve to be discarded.

The report mentions, but does not deal adequately with, the studies suggesting the "beneficial" effects on the primary teeth of the fetus in women receiving fluoride supplements. Leverett of the Eastman Dental Center, Rochester, New York, showed that Glenn's studies were incompetently carried out and that when he (Leverett) completed a well designed study, the results showed conclusively that there was no difference in caries incidence or pregnancy outcome between the supplemented group and the control after five years.(13) Unfortunately, Leverett "on ethical grounds" gave both groups of children supplements after five years thereby sabotaging his own experiment. This experiment showed clearly the lack of benefit from strictly systemic use of fluoride.

There is no reference in the report to recently published work that suggests that low levels of fluoride delivered to the fetus through the placenta may cause brain damage resulting in behaviour disorder or low IQ. (14-16) They omit also recent evidence that fluoride may contribute to infertility.(17)

When the authors of this report discuss the important subject of skeletal fluorosis, they present confusing calculations for the daily amount and time interval. In some respects, for example in their rehashing of the controversial "findings" of the Bartlett-Cameron study, they appear to be caught in a time-warp. The report presents both the calculation, now known to be erroneous, used in Health Benefits and Risks, 1991 (1), of "20-80 mg of fluoride per day for 10-20 years" and the now corrected value, found in the NRC/NAS Report of 1993 (2), of "10-20 mg of fluoride per day for 10-20 years." Because fluoride is cumulative, lower intake over a longer time period may result in crippling skeletal fluorosis. There are indications, therefore, that both the Adequate Intake (AI) and the Upper Intake Level (UL) values shown in Tables S5 and S6 of the report are set too high to prevent this serious complication. [emphasis added]

The authors selected a study that showed a total fluoride intake for adults of 1.4 - 3.4 mg/day in fluoridated areas (1 mg/L) and 0.3 - 1.0 mg/day in non fluoridated areas (<0.3 mg/L) (p 8 5). These estimates are lower than those presented elsewhere. For a 70 kg adult, a Health Canada survey (18) gives 3.22 - 4.06 mg/day in fluoridated and 2.24 - 2.45 mg/day in nonfluoridated areas; the US Public Health Service, in Health Benefits and Risks (1) 2.1 - 9.1 mg/day in fluoridated (0.7 - 1.2 mg/L) and 1.1 - 2.8 in non-fluoridated (<0.3 mg/L). It may be shown from these intake estimates, especially for fluoridated populations, that whether the NAS (1993) estimate for skeletal fluorosis (2) or Roholm's 1937 findings for cryolite workers (19) are used, skeletal fluorosis (osteosclerosis) is a major possibility. Roholm's estimates can be used to show that a daily fluoride intake of 3.5 6.0 mg/day could produce "recognizable sclerosis" after 37 years of exposure and "severe sclerosis" around the age of 84. At the UL of 10 mg/day fluoride intake, this problem could occur after a shorter time interval.

The statement that " there was no evidence that dietary fluoride intake in the 1970s and 1980s had increased over the 1950s" is not in accord with common sense and not supported by research. Kintner (20) reviewed this to 1991 and estimated that total fluoride intake for an adult in the U.S. had increased from 0.45-0.55 mg/day prior to 1950 to a mean of 2.7 mg/day in fluoridated communities in 1991. Horowitz (1992) (21) recognized the increase for residents of both fluoridated and non-fluoridated areas. Recently, studies have shown elevations of fluoride in juices, juice-flavoured drinks and frozen concentrates reconstituted with distilled water, sold in the US (Kiritsy 1996) (22) and in California wines contaminated by the pesticide cryolite (Burgstahler 1997) (23).


Once again, a report on fluoride (and fluoridation) is presented that is more propaganda than science. Supporters of fluoridation and the users of other fluoride " technologies" such as the American Dental Association, will obtain comfort from the "confirmation" that the cariostatic effects of fluoride have been given recognition as an indicator for the establishment of Adequate Intake levels, in spite of the inability of the authors to find data to show that fluoride is an "essential nutrient" or that there is contemporary evidence to prove that the systemic use of fluoride is effective as a cariostatic agent. The "new" hypothesis concerning the "benefit" of topical use, presented at length in this report, appears to be more conjecture than reality, representing an adjustment to the failed concept of the past that "rationalized" mass medication via the drinking water supply.

The "confirmation" that dental fluorosis is an "adverse cosmetic effect" rather than an "adverse functional effect" will be hailed by fluoride promoters as it fits well the preconceived notion. The "reaffirmation" that new bone formation from fluoride ingestion is a positive finding rather than a harbinger of calamity to come will also receive favourable notice. The possibility of increased risk of hip fracture and of skeletal fluorosis is minimized, either by omission or down grading present daily fluoride intake. The tables showing the Adequate Intake (AI) and Tolerable Upper Levels (UL) are calculated to defend the concept that current intakes are "necessary for good dental health" and are at levels that are "safe". This Institute of Medicine Report ignores a vast body of contrary evidence that undermines the seemingly sure positions that it seeks to impose on an unquestioning public. It makes a mockery of true science, which requires consideration of all relevant data before reaching conclusions.

There is some truth in this report; but, like the search for Waldo, the search for truth is made difficult to find amidst the background verbiage. What are these "truths"?

  • First, there is no evidence to show that fluoride is an "essential" nutrient or a "nutrient" as opposed to a "contaminant" of human diet.
  • Second, there is no solid evidence that the systemic use of fluoride is cariostatic. There is, also, little to support the "benefits" of topical application. Therefore, the term "Adequate Intake" is meaningless.
  • Finally, it cannot be hidden, even in this biased report, that there are many "red flags" that should serve as a warning that serious dental, bone and other adverse effects will become apparent as the future unfolds.

Note: The prepublication proof of the report, from the Institute of Medicine, National Academy of Sciences Press, Washington DC 1997, was used for this review.

  1. Review of Fluoride: Benefits and Risks. US Public Health Service, 1991.
  2. Health Effects of Ingested Fluoride. National Research Council, National Academy of Science, 1993.
  3. Investigation of Inorganic Fluoride and its Effect on the Occurrence of Dental Caries and Dental Fluorosis in Canada Final Report. Health Canada, Health Protection Branch, July 2, 1994.
  4. Foulkes RG. Review of Reference 3. Fluoride 28 (3) 146 148 1995.
  5. Brunelle JA, Carlos JP. Recent trends in dental caries in US children and the effects of water fluoridation. Journal of Dental Research 69 (special issue) 723 727 1990.
  6. Brunelle JA (Ed). Oral Health of United States Children. National and Regional Findings. US Public Health Service, 1987.
  7. Gray A. Fluoridation: Time for a new baseline? Journal of the Canadian Dental Association 10 763-764 1987.
  8. Colquhoun J. Fluorides and the decline in tooth decay in New Zealand. Fluoride 26 (2) 125-134 1993.
  9. Hodge HC. The safety of fluoride tablets or drops. In: Johnson T, Taves DR, Olsen TO (Eds). Continuing Evaluation of the Use of Fluorides. American Association for the Advancement of Science, Washington DC 1979.
  10. Fejerskov O, Manji F, Baelum V. The nature and mechanisms of dental fluorosis in man. Journal of Dental Research 69 (special issue) 692 700 1990.
  11. Fejerskov O, Manji F, Baelum V. Dental fluorosis - a handbook for health workers. Munksgaard, Copenhagen 1988 p 108.
  12. Lee JR. Fluoridation and hip fracture, according to the National Research Council report "Health effects of ingested fluoride". Fluoride 26 (4) 274 277 1993.
  13. Leverett DH, Adair SM, Vaughan BW et al. Randomized clinical trial of the effect of prenatal fluoride supplements in preventing dental caries. Caries Research 31 (3) 174-179 1997. Also: Leverett DH. Clinical trial of the effect of prenatal fluoride supplements in preventing dental caries. Final report. Contract No. 1 DE 32441, National Institute of Dental Research, Bethesda MD 1992.
  1. Mullenix PJ, Denbesten PK, Schunior A, Kernan WJ. Neurotoxicity of sodium fluoride in rats. Neurotoxicology and Teratology 17 {2) 169 177 1995.
  2. Li XS, Zhi JL, Gao RQ. Effect of fluoride exposure on intelligence of children. Fluoride 28 (4) 189-192 1995.
  3. Zhao LB, Liang GH, Zhang DN, Wu XR. Effect of high fluoride water supply on children's intelligence. Fluoride 29 (4) 190 192 1996.
  4. Freni SC. Exposure to high fluoride concentration on drinking water is associated with decreased birth rates. Journal of Toxicology and Environmental Health 42 109 121 1994.
  5. Canadian Environmental Protection Act, "Inorganic fluorides", Cat no. EN 40 215/32E (Table 3). Ministry of Supply and Services, Ottawa 1993.
  6. Roholm K. Fluorine Intoxication. A Clinical-Hygienic Study. Nyt Nordisk, Copenhagen and H K Lewis, London 1937 pp 281 282.
  7. Kintner RR. Dietary fluoride in the USA. revisited (Guest Editorial). Fluoride 24 (1) 1-9 1991.
  8. Horowitz H. The need for toothpaste with lower than conventional fluoride concentrations for pre-school children. Journal of Public Health Dentistry52 (4) 216-221 1992.
  9. Kiritsy MC, Levy SM, Warren JJ et al. Assessing fluoride concentrationsof juices and juice-flavored drinks. Journal of the American Dental Association 127 (7) 895-902 1996.
  10. Burgstahler A, Robinson MA. Fluoride in California wines and raisins. Fluoride 30 (3) 142-146 1997.

IMMEDIATE RELEASE September 23, 1997

The document "Dietary Reference Intakes, Prepublication Copy" (DRI) is seriously flawed and deficient as an instrument to justify a public policy to establish fluoride as an "essential nutrient". The DRI document is rife with inadequacy, error and deceptive information, only some of which can be touched upon here.

For example, the only adverse effects of fluoride exposure discussed in DRI are enamel and skeletal fluorosis. These effects are only cursorily and deceptively touched upon, and no connection is made between them, as though they were independent effects and fluoride affinity for and damage to enamel is not a biochemical window on what is happening in bone.

While DRI lays out the parameters for conducting risk assessments in Chapter 3, it ignores application of those parameters particularly egregiously with respect to fluoride in purporting to establish a "tolerable upper intake level'. One component of risk assessment is hazard identification, whose components include addressing evidence of adverse effects in humans. DRI attempts to deceive the public into believing the only identified adverse effects of fluoride exposure of significance are those mentioned above. The DRI document omits any mention of studies in humans showing increased risk of hip fractures and bone cancer and decreased I.Q. in children in areas with artificially fluoridated water or other sources or dietary fluoride that result in fluoride intakes that are below the "tolerable appear intake". Neither does the DRI document properly address use of animal data in the hazard and risk assessments on fluoride. There are recent (1990-1995) animal data supporting concern for both cancer and central nervous system effects.

Even if one grants as accurate the statement at page 8-15 in the prepublication copy of DRI, "Most research has indicated that an intake Or at leat 10 mg/day for 10 or more years is needed to produce clinical signs of the milder forms of the condition" (skeletal fluorosis), consider the simple mathematics of this "tolerable upper intake" level. That level is set at 10/mg/day for individuals aged 9 years and up. At age 39, the individual who has received the "tolerable upper intake" since age 9 will have accumulated 3 times the amount of fluoride needed, according to the DRI, to put him or her at high risk or skeletal fluorosis -- not to mention bone fracture, cancer and decreased mental capacity.

When a chemical manufacturer wants to make a new chemical to use, for exempt-, as an additive in motor oil, all existing toxicological data must be presented to the Environmental Protection Agency for review of potential risks before manufacture and use can begin. In the DRI we see risk assessment principles, as applied to a major public policy issue, flouted -- even the existence of a massive body of information on adverse effects of fluoride is ignored, let alone discussed And this for a chemical the National Academy recommends we purposely add to our diets, not our motor oil.

Furthermore, the claimed benefits from the "adequate intake" level have been shown to be based on biased or otherwise flawed studies. Not a single one of those studies was a randomized control trial.

In summary, our union members' review of the literature over the last 11 years has led us to conclude that a causal link exists between fluoride exposure and cancer, increased risk of hip fracture, and damage to the central nervous system. For the National Academy of Sciences to attempt to anoint this substance an "essential nutrient" is a travesty and a matter of shame for the U. S. science community.

National Federation of Federal Employees Local 2050 represents and is comprised of scientists, lawyers, engineers and other professionals at Headquarters, U S Environmental Protection Agency Washington DC

Central Nervous System References: 
  1. Li, X S , Zhi, J L , Gao, R. O. Effect of fluoride exposure on intelligence in children. Fluoride 28:4, 189-192 (1995).
  2. Zhao, L.B., Liang, G., Zhang, D., Lu-Liang, X. Wu, Effect of a high fluoride water supply on children's intelligence. Fluoride 29:4, 190-192 (1996).
  3. Mullenix, P.J., Denbesten, P.K., Schunior, A., Kernan, W.J. Neurotoxicity of sodium fluoride in rats. Neurotoxicology and Teratology 17:2, 169-177 (1995)

CONTACT: Dr. J. William Hirzy, Senior Vice President 202-260-4683
Distributed in Canada, for NFFE by Health Action Network Society, Alberta Chapter


JANUARY 19, 1973: The Food and Drug Administration (FDA), within the framework of proposing new rules, published a list of several nutrients which were termed essential but for which no Recommended Daily Allowances (RDAs) were established. Fluorine (fluoride)* was included in this list. (Federal Register, 1/19/73, page 2149)

AUGUST 2, 1973: Fluoride officially classified as essential by the FDA. (Federal Register, 8/2/73, page 20717; also appeared in 1974 Code of Federal Regulations (CFR), Title 21, Par. 125.1(c). Notwithstanding, the classification of essential given to fluoride, dietary supplements contained fluoride, were, and still are, available only on prescription.

1974: As a result of court action challenging some of the FDA policies and regulations, the Court directed the FDA to integrate the nutrients classified as essential but not having RDAs, into the Code of Federal Regulations (CFR), so as to be available for addition to general purpose foods or as over-the- counter dietary supplements. (National Nutritional Foods Association (NNFA) vs. FDA, 504 Federal Reporter 2d page 786; Court of Appeals, Second Circuit, decided 8/15/74).

May 28, 1975 Federal Register, 5/28/75, page 23248:

  • (a) FLUORIDE is explicitly designated by the FDA as not general recognized as safe . Earlier regulations already disqualified fluoride from the category of generally recognized as safe, but this was not directly stated before May 28, 1975. (Therefore, fluoride was never on the GRAS List, not because it did not happen to be considered -but because it was considered and found INELIGIBLE for the List due to concern about toxicity.)
  • (b) FLUORIDE is a FOOD ADDITIVE under the Federal Food, Drug & Cosmetic Act, because any vitamin or mineral which is not generally recognized as safe falls under this definition of a food additive.
  • (c) FLUORIDE is a food additive at any level, unlike many other substances which only become food additives if they exceed a certain level.

The FDA permits no fluoride whatever to be added to food or over-the-counter dietary supplements. However, the Department of Health, Education & Welfare (HEW) has, for many years, and to this date, exempted fluoridated water supplies from this FDA ban, as well as exempted the addition of such fluoridated water in the processing of food. (CFR, Title 21, 1979, Par. 170.45, Fluorine Containing Compounds ; (CFR, Title 21, 1979, Par. 250.203, Status of Fluoridated Water and Food Prepared with Fluoridated Water ). (These regulations have been in effect for many years.)

Note: Paradoxically, in 1975, at the same time that fluoride was classified as essential by the FDA, they also explicitly designated it as not generally recognized as safe at any level.

OCTOBER 19, 1976: Fluoride’s classification of essential was weakened from essential to essential or probably essential for which no RDA was established. (Federal Register, 10/19/76, page 46175; also CFR, 4/1/77 and 4/1/78, Paragraphs 105.3(c) and 105.85(d) (4).

1978: Court action -- where it was reaffirmed that any vitamins or mineral not generally recognized as safe had to be classified as a food additive under the Federal Food, Drug & Cosmetic Act; -- it was also disclosed that the FDA had failed to comply with court directive to permit inclusion of vitamins and minerals recognized to be essential to human nutrition, but for which no RDAs had been established, into general purpose foods or as over-the-counter dietary supplements (NNFA vs. Kennedy (FDA) 572 f 2d 377 (2nd Circ. 1978)

MARCH 16, 1979: FDA deleted Paragraphs 105.3(c) and 105.85(d)(4) of Federal Register which had classified fluorine, among other substances as essential or probably essential . Fluoride is no nowhere in the Federal Regulations classified as essential or probably essential. This deletions was the immediate result of the 1978 Court deliberations. (Federal Register, 3/16/79, page 16006.

MARCH 16, 1979: FDA deleted Paragraphs 105.3(c) and 105.85(d)(4) of Federal Register which had classified fluorine, among other substances as essential or probably essential.

*In this discussion, the words fluorine and fluoride are used interchangeably.

U.S. Public Health Service report of 1991
"Review of Fluoride Benefits and Risks"

"Although fluoride compounds occur naturally, both in the environment and in most constituents of the body, there is no conclusive evidence that fluorine or any of the fluoride compounds are essential for human homeostasis or growth."

1993 Statement by the National Research Council

"Health Effects of Ingest Fluoride", by a National Research Council Subcommittee, published by the National Academy Press, 1993:

"Although fluoride is no longer considered an essential factor for human growth and development (see NRC, 1989), many believe that there is an optimal dose of systemic fluoride for maximal benefit against caries." [emphasis added]
Note: The "belief" by fluoride proponents is just that -- a belief. It's not based on scientific research. Dental research has shown that fluoride's cariostatic mechanism is provided by topical applications to the teeth, such as found in fluoridated toothpaste. It's not achieved by ingesting it.

1971 Statement by National Academy of Sciences Committee

A Committee of the National Academy of Sciences (division of Medical Sciences National Research Council), in their publication "Biological Effects of Atmospheric Pollutants FLUORIDES", noted the following about dietary essentials:

"First, it should be possible to demonstrate repeated and significant responses in growth or health to dietary supplements of the element and to the element alone; second, it should be possible to develop a deficiency state on diets that lack the element but that are otherwise adequate and satisfactory. Such diets should contain all other known dietary essentials in adequate amounts."
"Unequivocal evidence that fluorides perform any vital function in animals has not yet been produced."

Regarding the oft-repeated claim by many proponents that fluoride reduces tooth decay and therefore is a nutrient, the Academy points out:

"That in itself is no indication of fluorine essentiality, inasmuch as caries incidence depends on many factors, and many persons with perfectly sound dentition have had only minimal exposure to fluoride."


"Guidelines For Canadian Drinking Water Quality Fluoride Supporting Documentation" (the Canadian federal-provincial subcommittee which just recently recommended lowering water fluoride levels to 0.8 ppm from 1.0 ppm):

"Although Health Canada classified fluoride as an essential element in the past, it now recommends that fluoride requirements can 'only be based on the beneficial effect on dental caries' and notes that 'attempts to demonstrate its essentiality for growth and reproduction in experimental animals have not been successful."

Home Fluoride: Protected Pollutant or Panacea?
Are the claimed benefits of ingesting fluoride over-rated
and the risks to our health and eco-system under-reported?
Scientific Abstracts
Bones | Calgary | Cavities | Fertility | Cancer | Health risks | Neurological | Dental Fluorosis and Pictures
ISFR | Ethics | Tributes | Fraud | Authors | Deaths | Quotes | Environment | Skeletal Fluorosis | Definitions

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