“Life” involves an incalculable number of chemically active molecules
initiating, continuing and terminating a bewildering variety of
chemical events. Throughout this panoply of events
and in every organ where they occur,
various enzymes play crucial roles.

Factors Often Overlooked In Fluoridation Research

– Research Papers – B

Last Update: 5th Dec. 2019

RESEARCH PAPERS 'B'

J. Westndorf

Westendorf'sResearch incomplete diss.

Full research paper  → HERE  

The oral defense took place on 2/18/1975

A Foreword intended to place the Westendorf research in current context indicating why it is relevant to a wide range of contemporary health and behavioral problems has been prepared by Myron J. Coplan and Roger D. Masters whose credentials are also attached.

Foreword by

M J Coplan and R D Masters, April 2001

West..Re 30year

Second, Westendorf’s research was based on knowledge that fluoride ion is an enzyme inhibitor. Indeed, that feature of ingested fluoride seemed to offer multiple benefits. Knappwost believed that ingested fluoride, by inhibiting cholinesterase, could achieve both greater expression of total saliva and an increase in its fluoride content. The research of his student quite logically examined different forms of ingestible fluoride for their effect on several variants of cholinesterase, Westendorf’s results showed that fluoride in the form of the silicofluoride complex (SiF), as well as several other complexes, was a substantially more powerful inhibitor of cholinesterases than the simple fluoride ion released by sodium fluoride (NaF). This was simply an objective finding.

Third, to account for the more powerful inhibition effect of SiF, Westendorf studied the course of its fluoride release in fine detail. He found that under physiological conditions, dissociation was no more than 66% in the concentration range considered “optimum” for fluoridated water by United States health authorities. If the released fluoride came uniformly from all of the initially injected SiF, the molar concentration of the residual non-dissociated species would be the same as that of the injected SiF. It would follow that dilution of fluosilicic acid to a nominal 1 part per million of free fluoride in water at pH 7.4 induces each [SiF6]2- to release 4 fluorides to be replaced by hydroxyls. The partially dissociated residue would be the ion [SiF2(OH)4]2- which would then be present in the water at the same concentration as the originally introduced SiF. The biological consequences of ingesting such a species are probably not innocuous, with enzyme inhibition being only one of several possibilities.

Westendorf’s visualized course of SiF dissociation, based on actual experimental evidence, is materially at odds with the dissociation route assumed by US EPA and CDC, based on theory. In judging the reliability of the theoretical approach and claims of health safety presented by these government agencies, one should be aware that both the nature of the complicated mixture called “fluosilicic acid” and the course of its dissociation upon dilution remain unresolved despite nearly a century of research. Two recent documents demonstrate this. In the first, an expert in the recovery of fluoride in phosphate rock processing, addressing a group of his peers at a 1999 International Fertilizer Association (a) meeting held in the former USSR, said:

“The chemical formula of fluosilicic acid is H2SiF6. However, things are not as simple as that due to the fact that rarely is fluosilicic acid present as pure H2SiF6. . . There are well reported references to the existence of H2SiF6 SiF4. . . Hereon in this presentation, FSA [fluosilicic acid] means a mixture of HF, H2SiF6 and H2SiF6 SiF4.”

This is a highly significant statement coming from someone who ought to know the subject under discussion. It means that a key intermediate dissociation product postulated by CDC and EPA theories to be transient species only fleetingly after SiF is introduced into the water at the water plant, may be present in concentrated fluosilicic acid before dissociation begins. Such a starting condition would cast serious doubt on the postulated theoretical equations predicting “virtually 100%” dissociation that supposedly “guarantee” no adverse health effects from undissociated SiF residues in drinking water treated with these compounds.

Equally important is a letter (b) dated March 15, 2001, written by the Director of the EPA Water Supply and Water Resources Division, which concludes with the statement:

“In January, representatives from the [EPA] Office of Research and Development (ORD) and the Office of Science and Technology and Ground Water and Drinking Water met to discuss a number of water related issues including Fluoridation. Several fluoride chemistry related research needs were identified including; (1) accurate and precise values for the stability constants of mixed fluorohydroxo complexes with aluminum (III), iron (III) and other metal cations likely to be found under drinking water conditions and (2) a kinetic model for the dissociation and hydrolysis of fluosilicates and stepwise equilibrium constants for the partial hydrolysis products.”

In plain English, senior EPA research staff now believe their staff needs to go back to the lab for at least another year or two to find out if the EPA’s longstanding confidence in the “virtually total” dissociation of SiFs may have been misplaced. Whatever the outcome may be of their new study of SiF dissociation, it is clear the EPA does not intend to perform animal tests to ascertain health effects of chronic ingestion of SiF treated water under controlled conditions.

Animal experiments according to accepted toxicology testing protocols would be the logical way to examine health effects of enzyme inhibition by SiF that Westendorf observed at the cellular level. Three published reports bearing directly on this matter should be noted. In the early 1930s, the Ohio agriculture department wanted to develop a replacement for bone meal as a source of calcium and phosphorus in the feed ration of farm animals. Natural “rock phosphate,” comprising largely calcium phosphate, was a candidate, but it was known to carry about 2 to 5% of fluoride bound in some chemical form. Thus it was necessary to study possible adverse health effects due to ingestion of fluoride from several sources.

A report (c) issued in 1935 compared health effects primarily from calcium fluoride, sodium fluoride, and rock phosphate. Highly significant for present purposes was one small experiment that included sodium fluosilicate. With equal dosage and equal amounts of fluoride retained, rats fed sodium fluosilicate excreted three times as much non-retained fluoride in urine as rats fed sodium fluoride, who eliminated more fluoride in feces. Apparently about three times as much fluoride had crossed the gut/blood membrane into the bloodstream from SiF than from NaF. A second report, this one by the US PHS, (d) was published about ten years after water fluoridation had begun. The study compared the time, starting from the date of fluoridation either with sodium fluosilicate or sodium fluoride, for urinary fluoride level to reach equilibrium with ingested fluoride from fluoridated water. The study populations were boys and men. There were two noteworthy results. First, for either fluoridating agent, urine fluoride levels in older males reached equilibrium with ingested fluoride levels sooner than in younger males. The longer time for young males can be accounted for by the fact that the weight of the older males was essentially constant, while the younger males were adding bone mass over the several years of the experiment. The bodies of younger males were therefore providing a time-related increase in storage compartment capacity for ingested fluoride.

A more important finding was that for the younger males it took longer for their urine level of fluoride to reach equilibrium with ingested water fluoride from SiF than from NaF. Apparently in growing boys SiF fluoride must have been metabolizing differently from NaF fluoride.

A third relevant study (e), conducted around the same time as Westendorf’s research, involved feeding water treated with the same fluosilicic acid used to fluoridate the local water supply to squirrel monkeys for up to 14 months. Morphological and cytochemical effects were reported for the liver, kidney, and nervous system due to ingestion of 1-5 ppm of fluoride in water. Although the study did not compare results from exposure to NaF, the report emphasizes the fact that the kidneys of monkeys ingesting SiF treated drinking water “Éshowed significant cytochemical changes, especially in the animals on 5 PPM fluoride intake in their drinking water.”

The report later observes that work by others in the 1940s and 1950s “Éshowed that fluoride has an inhibitive effect on the activity of succinate dehydrogenase. These studies indicate that under the effect of fluoride intake, a serious metabolic distress may develop in the kidneys.” In concluding, the report notes that “Earlier, some workers had also indicated that inorganic fluorides have a strongly adverse effect on the activity of some enzymes and of these, mitochondrial enzymes, acid and alkaline phosphatases and ATP-utilizing enzymes and aldolase may be the most affected (Batenburg & Van den Bergh, 1972; Katz & Tenenhouse, 1973).”

This study of squirrel monkeys is a rare (possibly singular) American experiment with SiF. If the research team had known that Westendorf was finding greater effects of silicofluoride than sodium fluoride on enzyme activity at virtually the same moment, the U.S. study might have taken a different turn. In any case, two of these three American experiments compared effects from NaF and SiF, and both found that SiF and NaF do not produce the same effect. Moreover, all three studies found the strongest adverse clinical effect of silicofluoride in the kidney. But damage to the kidney is hardly the only possible health effect of ingested SiF.

“Life” involves an incalculable number of chemically active molecules initiating, continuing and terminating a bewildering variety of chemical events. Throughout this panoply of events and in every organ where they occur, various enzymes play crucial roles. A particularly important example is the quenching by enzymes of muscle stimulation induced by the neurotransmitter acetylcholine (ACh), an ester comprising the acetyl moiety bound by an oxygen bridge to the choline molecule. The principal “quenching” enzyme, acetylycholinesterase (AChE), comes in several variations and the ACh/Ache dyads operate in numerous ways in many organs. Related enzymes called pseudocholinesterases are found in serum and include the butyrylcholinesterases.

At latest count over 7,000 enzymes have been detected and catalogued, (f) and there is no reason to suppose that the effect of SiF is limited only to a sub-class. In any event, one would be hard put to identify a more important enzyme subclass than “esterases,” which cleave molecules called “esters” at the right time and place in the healthy organism. While a great deal is known about many of the ways these enzymes function, there are still large knowledge gaps to be filled. To do just that, an extensive survey of contemporary knowledge about cholinesterases has recently been published (g) by an employee of the Office of Prevention, Pesticides and Toxic Substances in EPA’s Health Effects Division. The published article carries this disclaimer:

“Although this article was written as part of the author’s official duties as an EPA scientist, the opinions and conclusions expressed in it are his alone, and do not reflect the position of the Environmental Protection Agency.”

Dementi’s review deserves a great deal of attention, so one wonders why it was not published as official work of the EPA. The EPA has acknowledged (h) that it has no data on health effects of the SiFs, shown by Westendorf to be a significant cholinesterase inhibitor and being added to the diets of 140 million people at the rate of 200,000 tons a year. The many different biochemical responses this dosage can be expected to elicit may well support a recently published (l) hypothesis proposing an explanation for Fibromyalgia, Multiple Chemical Sensitivity, and Chronic Fatigue Syndrome. It is not at all unlikely that chronic ingestion of SiF treated water also bears on ADD/ADHD, teen violence, and even some of the ambiguities associated with Gulf War Syndrome.

Common sense suggests that wide-spread, albeit clinically vague, adverse health effects should be expected when a strong enzyme inhibitor is added to the daily diets of over half of US residents, as would be the case given the results of the research work described herein. With millions of people suffering from one or another poorly understood condition with likely roots in environmental toxins, it is time to re-examine entrenched governmental doctrines in the light of Westendorf’s research which, while 30 years old, has received little or no attention heretofore.

(Read Westendorf’s thesis)

Notes and Credits

NOTE 1. The following English language text, translated from the German in which it was written by Dr. Johannes Westendorf, (Toxicology Department, Eppendorf-Hamburg University Hospital) was submitted to him in March 2001 for his comments with a series of questions. This was his response.

“With respect to my thesis I finished this kind of work in 1976, when I changed to the Medical faculty, where I still am. After my thesis I continued the work on fluoride for another year and we especially worked on the stability of hexafluoro complexes of silicon and iron. We used radioactive isotopes, such as F-18 and Si-31 . . . when we analyzed the electrophoretic mobility. In the presence of silicon and iron, fluoride ions showed a different mobility compared to fluoride [ion] itself. Unfortunately I have no access to these old experiments and we did not publish it.

. . . During hydrolysis we got a continuous shifting of the mobility, indicating that the different forms of hydrolysis with 2-6 fluorine at the Si are present at the same time, ending up at the more stable form of Si(OH)4F2. If we increased the pH to 9 and higher, a total hydrolysis occurs.

…In answering your final paragraph I can say:

1) The English translation of my thesis is excellent.

2) I have no evidence from others that contradict to my old findings.

3) Your idea of the enzyme inhibition by the complex could be right, however slight changes in the pH, caused by the hydrolysis of hexafluorosilicate, would also result in an increased inhibition of acetylcholinesterase. Nevertheless, I agree with you that the toxicology of hexafluorosilicate should be investigated because it may be different from simple fluoride.

Please let me know if I can be of further assistance to you. Johannes Westendorf”

Westendorf@uke.uni-hamburg.de

NOTE II. Although the main body of the Westendorf thesis was not published in a circulating journal as such, three short articles based on this work were. Copies of the two most relevant ones appear at the end of the English text of the full thesis.

CREDITS: The thesis was called to our attention and photocopied from the document on file in the archives at the University of Hamburg by Peter Meiers (Weissenburgerstr. 28, D-66113 Saarbrucken; the translation was prepared by Jakob von Moltke (Dartmouth College); final proof editing was done by Myron Coplan with the aid of Norman Mancuso.

References:

a) Smith, PA. “History of Fluorine Recovery Processes”: Paper delivered at the IFA Technical Sub-Committee and Committee Meeting in Novgorord, Russia; Sept 15-17, 1999 (http://www.fertilizer.org/ifa/publicat/techpprs/tech0999.asp)

b) Gutierrez, SB. (signed by Thurnau RC); Letter from the Director of the US EPA National Risk Management Laboratory to Roger D. Masters, dated March 15, 2001.

c) Kick CH, et al. “Fluorine in Animal Nutrition”; Bulletin 558, Ohio Agricultural Experiment Station; Wooster, Ohio; November 1935; pp 1-77.

d) Zipkin, I et al. “Urinary Fluoride Levels Associated with Use of Fluoridated Water”; Pub Hlth Rpts 71 PP 767-772; 1956.

e) Manocha SL, et al. “Cytochemical response of kidney, liver and nervous system to fluoride ions in drinking water”; Histochemical Journal, 7 (1975); 343-355.

f) On February 7, 2001, the Brookhaven Registry of Enzymes listed 7,164 enzymes on their web-site, http://www.biochem.ucl.ac.uk/bsm/enzymes/

g) Dementi, B. “Cholinesterase Literature Review and Comment”; Pesticides, People and Nature; 1 (2); 59-126; 1999.

h) Letter to the Honorable Ken Calvert, Chairman of the Subcommittee on Energy and the Environment, US House Committee on Science, from EPA Assistant Administrator J. Charles Fox, June 23, 1999.

i) Laylander, J. “A Nutrient/Toxin Interaction Theory of the Etiology and Pathogenesis of Chronic Pain-Fatigue Syndromes: Parts I & II,” Journal of Chronic Fatigue Syndrome; 5(1), 67-126, 1999.

Synopsis of Foreword Authors’ Relevant Professional History

Roger D. Masters, Ph.D., is President of the Foundation for Neuroscience and Society and Nelson A. Rockefeller Professor of Government Emeritus at Dartmouth College. For the last 30 years, he has studied the implications of modern biological science in understanding human behavior. He serves as editor of the “Biology and Social Life” section of Social Science Information (an international journal published at the Maison des Sciences de l’Homme in Paris) and member of the Council of the Association for Politics and the Life Sciences. He is a published expert in the history of Renaissance politics, especially the contribution of Niccolo Machiavelli.

After undergraduate studies at Harvard (where his instructors included Henry Kissinger), he served in the US Army before graduate studies at the University of Chicago. Despite his work in other areas, he retained a strong professional interest in military and international affairs. In addition to writing The Nation is Burdened: American Foreign Policy in a Changing World (Knopf, 1967), he served as US Cultural Attache to France. Among his many other books are The Political Philosophy of Rousseau (Princeton, 1968), The Nature of Politics (Yale, 1989), Machiavelli, Leonardo, and the Science of Power (Notre Dame Press, 1996) and Fortune is a River: Leonardo da Vinci and Niccolo Machiavelli’s Magnificent Dream to Change the Course of Florentine History (Free Press, 1998). Before turning to issues of environmental pollution, health and behavior, he also published widely on the effectiveness of leaders’ nonverbal behavior on television (working with colleagues on experiments in France and Germany as well as in the US).

Among many other publications on biological factors in human behavior, he was co-editor (with Michael T McGuire) of The Neurotransmitter Revolution, Serotonin, Social Behavior and the Law (Southern Illinois University Press, 1994); senior author (with Brian Hone and Anil Doshi) of “Environmental Pollution, Neurotoxicity, and Criminal Violence,” in J. Rose, ed., Aspects of Environmental Toxicity (London: Gordon & Breach, 1998), pp. 13-45; and co-author (with MJ Coplan) of “Water Treatment with Silicofluorides and Lead Toxicity,” International Journal of Environmental Studies, 56: 435-449 (July-August 1999) as well as of other publications.

In addition to an earlier teaching position in political science at Yale, he served as US Cultural Attache to France, Fellow of the Hastings Center, Chair of the Executive Committee of the Gruter Institute for Law and Behavioral Research (a foundation specialized in linking biology to the study and practice of law), a visiting professor at Yale Law School and Vermont Law School, and a consultant to Upjohn Corp, to the Commissioner of Corrections of Vermont, and to several agencies of the Federal Government. As a result of these varied professional activities, Dr. Masters has had extensive experience applying new scientific research in biology of human behavior to the establishment of successful government policies.

Myron J. Coplan, PE is a consultant in chemical engineering and chemical sciences, doing business at “Intellequity” after retirement in 1987 as Vice President and General Manager of the Albany International Co. Membrane Development Venture. The fruits of this latter activity include a product line of membranes now used by a major multi-national company to supply a market for industrial gases measured in the $ billions.

Coplan’s working career started during WWII first as a civilian employee of the US War Department and then as a production chemist for a firm supplying the military with two crucial commodities: DDT, without which the S. Pacific campaign might not have been successful, and a wire insulating chemical, without which the US Navy’s capacity to deal with disastrous convoy damage by Nazi mines might not have been achieved. He was one of the few civilians deferred throughout WWII for his critical occupation status.

Post WWII, while pursuing his own advanced degree studies, Coplan headed an academic chemical engineering department, supervising doctoral research of others. This was followed by a 37-year relationship with an independent consulting and r/d firm specializing in material sciences (chemistry, polymer systems, statistical analysis, physics, fluid dynamics, statistical mechanics, etc.) which eventually became the central research laboratory of a large multinational corporation.

Coplan is recognized in American Men of Science, holds 32 patents, is a member of several professional organizations and has published many technical papers. He authored a series of bench-mark articles on mathematical probability statistics and wrote a manual on statistical quality control for internal corporate use. He also personally carried out a wide range of laboratory research and engineering tasks and supervised the work of as many as 35 other professionals of many disciplines. He has been consulted by research staffs and corporate executives from some of the world’s largest corporations. To mention only one example, over about ten years he had 28 assignments from GE.

His services were also engaged by NASA, USDA, EPA, Interior Dept, Post Office Dept and several other government agencies, including virtually every branch of the DOD. In these assignments, Coplan was cleared on a “need-to-know” high level security basis several times for consulting and research work in such diverse fields as “decoy” chaff used to frustrate radar-tracked anti-aircraft fire to protective measures for ground-troops at risk of exposure to chemical, biological and nuclear attack.

In due course, Coplan’s activities became more focused on the interests of the large company which in 1972 had acquired the firm he had joined in 1951. After 1972, he took on the corporate mission of identifying and exploiting science-based new business opportunities, including direct management of scientific entrepreneurial r/d for new products and technologies. He became Senior Corporate Scientist and then Vice President and General Manager of a membrane development venture that eventually licensed his patented inventions to other large corporations. Membrane treatment of phosphate waste pond waters was among the applications studied. Coplan, therefore, has first-hand knowledge of the processes from which the principal water fluoridating agents (the silicofluorides) are derived.

Full research paper → HERE  

Black Lines separate

FLUORIDE – The Aging Factor

HOW TO RECOGNIZE AND AVOID

THE DEVASTATING EFFECTS OF FLUORIDE

J.A. Yia...

John A. Yiamouyiannis, Ph.D. (1943-2000)

At the center of the second-generation conspiracy is John Small. While he is only a high school graduate with no college degree, his credentials do include six years as an information officer for a government department on chemical warfare. He is now and has been the U.S. Public Health Service ‘expert’ on fluoridation since the 1960s.

fluoride/fluoride/fluoridation/fluoridationyiamousyiannis

Mr. Small’s functions at the USPHS [United States Public Health Service] include the writing and printing of anonymous memos, on USPHS letterheads, covering up the harmful effects of fluoridation, and distributing these memos to promoters of fluoridation, and when necessary, getting his hands on memos and reports put out by the government (even the White House) and rewriting them so they no longer express their original concerns about the toxicity and ineffectiveness of fluoridation. Most of the information supplied to dentists and physicians concerning fluoridation comes either directly or indirectly from Mr. Small. He is the cover-up supervisor, an expert relied upon by the USPHS to supply answers to Congress.

He also has the task of harassing, intimidating, and destroying anyone whose publications, utterances, or activities work to the detriment of fluoridation. In some cases, he calls upon other divisions of the Public Health Service to ‘neutralize’ studies or articles showing adverse effects of fluoridation.

In 1969, when Dr. Yiamouyiannis was a biochemical editor for Chemical Abstracts Service, the world’s largest chemical information center and the largest division of the American Chemical Society, he began to publicly express his concern about the health risks associated with fluoridation.

Mr. Small contacted his employer and communicated his displeasure with the statements of Dr. Yiamouyiannis. Dr. Yiamouyiannis was notified by his employer several times and finally told that if he spoke out against fluoridation one more time, he would be fired. He was told that $1.1 million in federal funding was in jeopardy if Chemical Abstracts Service did not shut him up.

After the meeting, his employer wrote to Small, “I have again talked to Dr. Yiamouyiannis and I have again made my position as strong and as clear as possible. He will not repeat this kind of performance and remain as an employee of Chemical Abstracts Service.” Within weeks after Dr. Yiamouyiannis next spoke out against fluoridation, he was put on probation, was told that he would never receive a raise again, and was advised to find another job. He was ultimately forced to resign.

Two years later, Dr. Yiamouyiannis was appointed science director of the National Health Federation where he was able to devote more time on the fluoridation issue.

During the 1970s, the fluoridation battle was stalemated. On one side, those opposing fluoridation were winning elections to stop fluoridation. On the other side, there was the force and money and power of the USPHS, the ADA, and industry that kept fluoridation going. In 1978, Yiamouyiannis served as a consultant and witness in a court case in Pennsylvania that proved fluoridation was harmful and banned it. The fluoridation promoters had to do something.

ADA’s White Paper

In 1979, the American Dental Association came out with a “White Paper on Fluoridation” characterizing fluoridation opponents as either “uninformed or misinformed” or “self-styled experts whose qualifications for speaking out on such a scientific issue as fluoridation were practically nonexistent or whose motivation was self-serving.” It suggested that dentists should propagandize politicians while they are in the dental chair. The White Paper proposed setting up the conspiracy between the American Dental Association, Centers for Disease Control, Environmental Protection Agency, National Center for Health Statistics, National Institute of Dental Research, state dental societies, and state dental directors for “identification of communities where the timing for political action is favorable as well as unfavorable and where the opponents of fluoridation are considering the initiation of referendums” and for “promoting fluoridation.”

It urged that “individual dentists must be convinced that they need not be familiar with scientific reports . . . on fluoridation to be effective participants in the promotion program” and that the ADA should cooperate with the USPHS to get EPA to soften its statements regarding fluoride as a contaminant. It suggested behavioral studies to “help anticipate the behavior of opponents of fluoridation,” e.g. studies that would determine “Why would some persons deny the life-long health benefits of fluoridation to children? What kind of mentality would reject the opinion of those who are qualified by education, training and experience . . .”

It suggested that ADA’s responses to opponents of fluoridation should be prefaced by: “The ADA reiterated its longstanding support of fluoridation . . . Numerous studies have shown . . . There is no evidence of any relation . . . Investigators have observed . . . .” It suggested that “The advice of behavioral scientists should be sought with regard to more realistic, convincing rebuttals” and that “The ADA should produce a step-by-step manual for the development and conduct of a fluoridation campaign . . . The ADA should provide field assistance if needed in a fluoridation campaign or cooperate with the [US]PHS and state health departments in providing such assistance.”

Strategies of the Second Generation

This conspiracy solidified in the formation of a planning committee to organize a symposium (sponsored by the United States Department of Health and Human Services (USDHHS), USPHS, Health Resources and Services Administration, Bureau of Health Care and Assistance, Maternal and Child Health Division, Centers for Disease Control, Center for Prevention Services, Dental Disease Prevention Activity, the W. K Kellogg Foundation, Delta Dental Health Plan of Michigan, Blue Cross and Blue Shield of Michigan, and Medical Products Laboratories). This symposium took place at the University of Michigan on August 9-10, 1983.

Members of the planning committee included Mr. Small, Mr. James Collins of the CDC, Dr. Stephen Corbin of the USPHS, Dr. Robert Mecklenburg, Chief Dental Officer of the USPHS, Dr. William Warren, Chief Dental Officer of the Department of Health and Human Services, Dr. Joel Boriskin, chairman of the American Dental Association’s National Fluoridation Advisory Committee, Dr. Wilbert Fletke of the ADA, Dr. Anthony Kiser of the ADA, Ms. M. Lisa Watson of the ADA, Ms. Martha Liggett of the American Association of Dental Schools, Dr. Michael Easley, formerly of the Ohio Dept. of Health and CDC, and Dr. Ray Kuthy of the Illinois Department of Health, who were and/or are some of the central figures in the conspiracy.

The stated purpose of the meeting was to “discuss the status of organized opposition to fluoridation; to analyze probable motives influencing the anti-fluoride movement; to assess the need for a national fluoridation strategy; to develop political and legal strategies for the defense and promotion of fluoridation; and to evaluate past legal and political pro-fluoridation initiatives, focusing on the defeats as well as the victories.”

An examination of the seminar speakers, their affiliation, and the content of their presentations provides a further look into the “un-American” nature of this taxpayer-supported event.

Speakers included:

Dr. William T. Jarvis, a member of the board of advisors of the American Council on Science and Health (ACSH) and the National Council Against Health Fraud (NCAHF). He spoke on the “Psychology of Anti-fluoridationism.” With regard to those opposing fluoridation, he stated: “I do not believe in providing such people a public platform from which they can create confusion and doubt about fluoridation . . . For several years I have put on fluoridation debates in my dental classes, taking surveys before and after to determine attitudes toward fluoridation. Invariably, each class became more anti-fluoridationist as a result of the debate.”

Dr. Sheldon Rovin, a member of ACSH and coauthor with Stephen Barrett of the book, The Tooth Robbers, a book defaming anti-fluoridationists. He spoke on how to win fluoridation battles through the political process, pointing out that “if it is at all humanly possible, the referendum should be avoided.” In the discussion following, Dr. Myron Allukian asked what could be done to stop anti-fluoridationists from getting signatures to put fluoridation on the ballot.

Dr. Stephen Corbin of the USPHS. As chairman of his workshop, he reported that his committee felt “the lead entities, namely the U.S. Public Health Service and the American Dental Association” should accept a plan “to close the ‘windows of vulnerability’ in our defense.” He suggested avoiding trials based on the merits of fluoridation. Finally, he suggested that a mandatory state fluoridation law be developed. During the following discussion, Dr. Easley suggested a conspiracy to deny those seeking relief through the courts their right to due process.

Dr. Dennis H. Leverett of the University of Rochester. As chairman of his workshop, he reported that his committee felt that fluoridation was “a political rather than a scientific situation” and encouraged research on the adverse effects of fluoridation “that will presumably show no effect or will show equivocal results.”

Dr. D. Scott Navarro of Blue Cross/Blue Shield, as chairman of his workshop, suggested that the cost of litigation defending fluoridation should be borne by taxpayers, professional organizations, health groups, universities, and research institutes.

Colleen Wulf of the Ohio Department of Health. As chairman of her workshop, she reported that her committee suggested the formation of a nonprofit organization which would coordinate with the CDC and ADA, pointing out that CDC has already drafted promotional materials for fluoride and that the ADA and the USPHS had already formed the Ad Hoc Committee to Plan for the Legal Defense of Community Water Fluoridation. She suggested that the name of the new group might be something like “Coalition for Improved Dental Health or something similar.”

ASLAP

As a matter of fact, the name of the group ended up being the American Oral Health Institute, incorporated in the state of Ohio on February 19, 1985 as a not-for-profit corporation. In 1985 and 1988, this organization came out with the first and second editions of a book, titled Abuse of the Scientific Literatune in an Antifluoridation Pamphlet (ASLAP), edited by Coleen A. Wulf, Karen F. Hughes, Kathleen G. Smith, and Michael W. Easley. The 215-page second edition of this book attacked the 1982, 1983, 1986, and 1988 editions of a very well referenced Question and Answer pamphlet titled Lifesavers Guide to Fluoridation by Dr. Yiamouyiannis that was effectively being used to fight fluoridation.

The preparation of this book was a collaborative effort of 18 federal and state health officials who were promoting fluoridation. Those with an asterisk after their name were invited to or attended the University of Michigan on August 9-10, 1983 symposium discussed above. There was not a single scientist among them: 10 were dental hygienists (Colleen A. Wulf*, Karen F. Hughes*, Kathleen G. Smith*, Linda S. Crossett*, Elizabeth King, Sharon Pierce, Ruth Nowjak-Raymer, Beverly Wargo, Geraldine Wirthman, and Karen Zinner), 2 were dentists (Michael Easley* and Elizabeth Bernard), 5 had degrees in public relations, education, psychology, or public health (James Collins*, Taimi M. Carnahan*, Claire Gelband, Judy Harvey, and Helen S. Hill), and one had no college degree at all (John Small*). The person who wrote the introduction was a psychiatrist (Stephen Barrett). . .

page 186

Consumer Reports

With the help of fluoride promoters, Consumer Reports prepared and published a two-part article on fluoride in its July and August 1978 issues. The writer of these articles was Mr. Joseph Botta. Mr. Botta holds a Master of Arts Degree in English, but no scientific degree. In this article he passed along the same lies and slander used by the promoters to the trusting readers of Consumer Reports.

The Consumer Reports article on fluoridation is the most artfully written piece incorporating the lies and slander necessary to discredit the research and personalities of scientists showing that fluoridation is harmful. It is by far the Number One article distributed by the government bureaucrats in their promotion of fluoridation. This is not because government bureaucrats are not skillful liars. It is because, by having their spoon-fed material rewritten and published by a “consumer” magazine, their lies become more believable. Dr. William Bock of the Centers for Disease Control thought it was so good that he ordered 10,000 reprints and paid for them with federal tax dollars. The American Dental Association gave Mr. Botta an award for writing it.

This Consumer Reports article was used by U.S. Public Health Service bureaucrats to provide a “scientific” foundation for their views on fluoridation. The situation has become ludicrous. For example, Dr. Vernon Houk, the director of the Environmental Center for Health of the Centers for Disease Control, traveled all the way from Atlanta, Georgia, to St. Paul, Minnesota, to give his “expert” testimony by reading from the Consumer Reports article.

The “Big Lie” in this article and the phrase most often quoted from it is the claim that “The simple truth is that there’s no “scientific controversy” over the safety of fluoridation.” In 1990, Dr. Edward Groth III, the technical director for Consumer Reports, nullified this claim by stating: “The point is that this is a legitimate scientific controversy. Proponents of fluoridation insist that there are no grounds for controversy at all, and with that, I totally disagree.” This hasn’t stopped proponents from quoting the same phrase to this day.

Who is Stephen Barrett?

Dr. Stephen Barrett, a psychiatrist, helped in the preparation of the 1978 Consumer Reports article and of the 1988 book Abuse of the Scientific Literature in an Antifluoridation Pamphlet. He has close ties with the American Dental Association, the American Medical Association, and the U.S. Public Health Service. He is a recipient of the FDA award for “quack-busting” and is a coauthor, along with William Jarvis and others, of the 1993 book Readers’ Guide to Alternative Health Methods, published by the American Medical Association. In this book, he cites, and gives summaries of, the two publications mentioned above to inform his readers about fluoridation. He is a science and editorial adviser to the American Council on Science and Health.

A glimpse into his character can be gained through his habitual use of words to mean their exact opposite. For example, in an article entitled “Poison Mongers,” Dr. Barrett refers to people who are trying to stop the addition of fluoride, a poison, to the water supply as poison-mongers. Now a monger is one who sells something, e.g. a fishmonger is a person who sells fish. Therefore, it is quite evident that a poison-monger is a person who sells poison. Thus, one opposed to having fluoride added to the water supply is exactly the opposite of a poison-monger. The word usage of Dr. Barrett is comparable to the process called “Newspeak” described in George Orwell’s 1984, where what is true becomes false and what is false becomes true. The first few paragraphs of Dr. Barrett’s article “Poison-Mongers” is the best example of how Dr. Barrett has used “Newspeak.” “In hundreds of American communities citizens have voted against healthier teeth.

“Why?

“They were confused by poison-mongers.

“These alarmists in our society are using confusion and a scare vocabulary as weapons against fluoridation. They are cheating all of us, but especially our children.

“The benefits of fluoridation are supported by 10,000 scientific studies which prove the poison-mongers are wrong.

“What do the poison-mongers say?

“Instead of telling you that fluoride is found naturally in all water, they call it a ‘pollutant’.

“Instead of telling you that fluoride is a nutrient essential to life, they call it a poison’.

“Instead of the big truth, that fluoridation has never harmed anyone, they tell the big lie and say it causes hundreds of ailments.”

This article was published in newspapers across the country and was printed in the November 1976 issue of the Journal of the American Dental Association. It has also been used by the U.S. Public Health Service in its ‘education’ of Congressmen and in its campaign to get various areas around the country fluoridated.

A closer look into Dr. Barrett’s personality can be obtained by examining his correspondence in 1972 with a group of people in Minnesota interested in stopping fluoridation. On March 8, 1972, Dr. Barrett wrote to one of these people, saying:

“I read your letter in Prevention [magazine] with some interest. There have been other attempts to defeat the fluoridationists in court but most have failed. Before investing money, I would like to have full details of what you plan.”

Thanks, Stephen J. Barrett, MD.”

In another letter to these people, dated April 4, 1972, Dr. Barrett wrote:

“Thank you for your recent telephone call. I am sorry that I could not immediately make the financial commitment which you requested. I know how enthusiastic you are and did not want to raise your hopes until I had a chance to discuss the matter with my group.

I am part of a group which is vitally concerned about fluoridation and which has raised a considerable amount of money. We are not yet sure whether it would be more practical to lobby or to go to court in Pennsylvania. The reason your lawsuit interests us is because it might be more practical for us to join your effort rather than go it alone.

“Thus we would need to have a detailed, written description of the plans of your suit. Our attorneys would then be in a position to study how it would effect Pa. law and also to estimate the chances of your suit being successful. We would also need some detail as to how the Attorney General’s favorable attitude will be used to advantage without this becoming apparent to the American Dental Association.

“We realize you are hesitant to say too much about your plans. On the other hand, we could not make a total commitment unless we had full knowledge of what we would be getting for our investment. We realize this asks a lot of you. On the other hand, we think we have a lot to offer.

“You may be assured that whatever information you send us will be handled with appropriate discretion.

“Sincerely yours, Stephen Barrett, M.D.”

On April 12, 1972, he wrote another letter to Miss Mary Bernhardt, the person at the American Dental Association responsible for promoting fluoridation, and related the following:

“Dear Miss Bernhardt:

“At about 6:20 this evening, I received another phone call from Mike Liptak, the organizer of MOFF [Minnesotans Opposed to Forced Fluoridation]. He said that at 4.30, Judge Gordon McRae ordered an injunction ‘to keep the fluoride out of Brainerd.’

“He said that there were 1500 people who watched the trial and that the judge had cautioned them about becoming emotional. They were very quiet. The case presented by MOFF included an affidavit from Dr. Waldbott. The attorney general of Minnesota defended and was given ‘five days for rebuttal.’ According to Mr. Liptak, who again said he went to school with the attorney general, the attorney general said he ‘would not furnish a rebuttal’. He merely stated that the new Minnesota law required fluoridation.

“Mr. Liptak added that there was an additional legal action scheduled for September. In about two weeks, 500 local citizens were planning to gather at a meeting where the vice-president of a local bank would get from them ’3 year notes for $50 each’ to help finance the suit. He explained that such mass action would not get them much publicity in Prevention magazine and the National Health Federation. It was their plan to seek further injunctions of this type with eventual overturning of the new state laws. He again asked me for a contribution, even a token one. He added that there might be money left over for use in another state such as Pennsylvania.

“On 5/14, Dr. Gross will try to contact leaders of the pro fluoridation forces in the Minnesota Dental Society and will also call the American Dental Association attorney. We have Mr. Liptak’s confidence and hope to continue to use it to our advantage. Perhaps the dental society should consider entering the suit as a guardian of the children. It might also be helpful if some quick way could be devised to dissuade the Brainerd residents from their imminent investment in foolishness.

“Best wishes, Stephen Barrett, M.D.”

Ironically, Dr. Barrett is a co-founder of the National Council Against Health Fraud.

Subsequently, he and Mary Bernhardt got together and published a book called The Health Robbers, in which they refer to those opposing fluoridation as health robbers. Excerpts from this book, which consist primarily of the substance of his poison-monger article, were reprinted in newspapers around the country, as well as in Family Health Magazine.

Teaming up with others of his kind, including Drs. Thomas Jukes, Warren Winklestein, and Joel M. Boriskin, Dr. Barrett complained about and tried to prevent Dr. Yiamouyiannis from speaking before the Faculty Club of the University of California, Berkeley. Together they claimed that Dr. Yiamouyiannis was some disreputable person not deserving a forum at the University of California campus.

In another action, Dr. Barrett, Dr. Boriskin and Dr. William Jarvis, who also is on the board of the National Council Against Health Fraud, wrote letters of complaint to the National News Council concerning an article published in the National Inquirer which pointed out that higher cancer risks were associated with fluoridation.

An indication of how Barrett’s ‘Newspeak’ is passed down the line to local dentists is evident from the experience Dr. Yiamouyiannis had when he was called in by local residents of St. Charles, Missouri for a debate on fluoridation. When Dr. Michael Garvey, a local dentist, heard that Dr. Yiamouyiannis was going to be the opposition speaker, he refused to participate in the debate.

According to the November 12, 1982 St. Charles Post: “Dr. Garvey said American Dental Association Officials had told him, ‘running up against Dr. Yiamouyiannis is not recommended’. The man is well-known as an antifluoridation speaker, Dr. Garvey said. ‘This guy is a terror.’”

page 203

Why haven’t Consumer Reports, Stephen Barrett and others who issue false and defamatory statements been sued for libel and slander? Why haven’t bureaucrats responsible for illegally spending tax monies to influence elections been prosecuted and sent to jail? Why haven’t bureaucrats who have lied in court while under oath been prosecuted for perjury?

In many cases they have. However, when legal action was taken against Consumer Reports, the court didn’t even allow a hearing on the case. The court claimed Consumer Reports’ right to freedom of speech outweighed the plaintiffs right to due process of the law.

When charges concerning Dr. Schneiderman’s alleged perjury in the Pittsburgh court case were brought before the district attorney’s office, they pointed out it would be virtually impossible to convict anyone on perjury and they rarely, if ever, prosecute such cases.

Dr. John Yiamouyiannis was not the first in the controversy over fluoridation. Even such accomplished physicians as Drs Ionel F Rapaport and George L Waldbott were severely oppressed in the early stages of the dispute over fluoridation. Even today, similar reprisals continue, as can be seen in the case of Forsyth Dental Research Center toxicologist Phyllis J Mullenix, phd, and USEPA cancer scientist William Marcus, phd. These actions are described by Professor Paul Connett in his “Fluoride: A Statement of Concern”, which is translated into Japanese in this issue of the Journal of the Japanese Society for Fluoride Research, as “a sickening thread that runs throughout this sorrowful 50-year history of fluoride promotion by the agencies of the US Public Health Service.”

Dr. John Yiamouyiannis, biochemist and founder of the Safe Water Foundation, USA, died October 8, 2000, passing away peacefully in sleep at his home in Delaware, Ohio, surrounded by members of his family.

 Health Action Press

6439 Taggart Road
Delaware, Ohio 43015
First edition published 1983
Third edition published 1993

Excerpts from the book,
with permission from the author.
Chapter 17 … THE CONSPIRACY:
The Second Generation

In 1975  Dr. John Yiamouyiannis publishes a preliminary survey which shows that people in fluoridated areas have a higher cancer death rate than those in non-fluoridated areas. The National Cancer Institute attempts to refute the studies. Later in 1975, Yiamouyiannis joins with Dr. Dean Burk, chief chemist of the National Cancer Institute (1939-1974) in performing other studies which are then included in the Congressional Record by Congressman Delaney, who was the original author of the Delaney Amendment, which prohibited the addition of cancer-causing substances to food used for human consumption. Both reports confirmed the existence of a link between fluoridation and cancer. (Note: Obviously Dr. Burk felt free to agree with scientific truth only after his tenure at NCI ended, since his job depended on towing the party line).In 1989 Dr.Yiamouyiannis used the Freedom of Information Act to obtain carcinogenicity studies conducted by Proctor and Gamble (one of the makers of fluoridated toothpaste) that were submitted to (and covered up by) the United States Public Health Service. These studies showed dose dependent cell abnormalities caused by fluoride. These results were reported in the February 22, 1990 issue of the Medical Tribune. Additional studies by Proctor and Gamble scientists confirmed the link between oral precancerous growth and fluoride, as well as an increase in  osteomas (bone tumors) and osteosarcomas (bone cancer). In fact, the National Cancer Institute found in 1991 that  the incidence of bone cancer was 50% higher in men ages 0-19 years of age exposed to fluoridated water compared to those who were not.

‘Quackwatch’ – Dead In The Water
DR. Stephen Barrett a Proven Quack!
From our →  Rouges Gallery 

Quackpot

Dr. Stephen Barrett of Quackwatch
Exposed In Court Cases:

At trial, under a heated cross-examination by Negrete, Barrett conceded that he was not a Medical Board Certified psychiatrist because he had failed the certification exam.

This was a major revelation since Barrett had provided supposed expert testimony as a psychiatrist and had testified in numerous court cases. Barrett also had said that he was a legal expert even though he had no formal legal training.

The most damning testimony before the jury, under the intense cross-examination by Negrete, was that Barrett had filed similar defamation lawsuits against almost 40 people across the country within the past few years and had not won one single one at trial.

During the course of his examination, Barrett also had to concede his ties to
the AMA,  FTC (Federal Trade Commission) and the FDA
(Food & Drug Administration)… [ say no more ]

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 ❝ VITAMIN ‘C’ AND FLUORIDATION ❞

by
John A. Yiamouyiannis, Ph.D. (1943-2000)

Yiamouyiannis ff

The National Health Federation
P.O. Box 688, Monrovia, California 91017
e-mail: contact-us@thenhf.com

Washington,  D.C.,  20002

Abstract: Vitamin C plays an important role in the orderly deposition of fluoride into various tissues. In higher fluoride areas, Vitamin C increases fluoride excretion and normalizes soft and hard tissue fluoride levels and thus prevents the development of fluorosis.  At lower fluoride levels, Vitamin C increases the incorporation of fluoride into teeth.  Fluoridation of water systems in not the solution to optimal incorporation of fluoride into teeth; in cases of Vitamin C deficiency, fluoridation may lead to fluorosis.

(21)          Hardwick & Bunting, J. Dent. Res. 50 (Supplement, Pt. 1), 1212 (1971)

– 7 August 1974 –

While fluoridation of public water systems has been advocated and encouraged by the national and state public health services, a number of questions concerning the need to add fluoride to public waters have gone unanswered.

Mother’s milk, containing as little as 0.01 to 0.05 ppm fluoride confers as much caries resistance on the child as other infants consuming 1 to 2 ppm fluoride present in commercially prepared formulas (1, 2).

In unfluoridated areas, containing natural fluoride levels of 0.1 to 0.5 ppm and even less, there exists a certain part of the population that are free of caries.  In fact, in Nigeria, a population has been found where over 98% of the population is caries free and the fluoride level in their water is within the above range (3).

In a study at Great Lakes Naval Base, the previous life-long residence of caries-free recruits, were examined to determine if any trace elements could be correlated with the low incidence of caries.

The level of fluoride in the drinking water was not implicated.

It has also been noticed that primitive areas in which the people of the area eat unrefined food have a relatively low caries rate as compared to later when these areas became “civilized” and their diets begin to consist of more refined foods.

In these cases, caries rates often soar and addition of fluoride to the water supply is unable to restore the previous caries rate (5, 6, 7).

In areas and among people where nutrition is poor, mottling is observed at levels below the 1 ppm level used to fluoridate public water systems (at levels as low as 0.4 ppm fluoride).

This has been noticed in India (8) as well as among American Negroes whose mottling rate, in the 1-ppm range is higher than that of whites in the same area.

In a comprehensive study in Japan, the fluoride levels associated with the lowest incidence of caries ranged from 0.2 to 0.4 ppm  (9).

In the 1930’s it was found that the ingestion of fluoride causes scurvy-like symptoms and that this was associated with a decrease in the Vitamin C levels of various tissues. Similarities in the symptoms of scurvy and mild fluorosis were also observed  (10, 11).

In 1954, in an area containing 0.34 to 0.8 ppm fluoride in the water, 23% of the children 4-7 years old exhibited mottling (dental fluorosis). The Vitamin C contents in blood for normal children (without mottling) averaged 0.78 mg %. In the mottled enamel group, the blood Vitamin C levels of most children were extremely low (0.15 to 0.3 mg % in 29%, and 0.0 to 0.15 mg % in 31%. Treatment of these subjects with Vitamin C brought substantial improvement  (12).

In 1964-65, the death rate of guinea pig population in Australia had reached epidemic proportion. (The Guinea pig is the only non-primate known that cannot synthesize its own Vitamin C). This death rate was eventually attributed to slightly higher levels of fluoride in feed pellets. Symptoms of sub-acute Vitamin C deficiency were observed. Fluorosis was diagnosed as the cause of death (13). In rats and mice (both of which synthesize their own Vitamin C, no such death rate was reported. U.S.P.H.S. experiments are performed with rats – they do not use guinea pigs (14). Both in the U.S. (15) and Russia (16) Vitamin C is recognized as being capable of retarding the development of fluorosis.

In guinea pigs exposed to fluoride, Vitamin C was found to normalize altered blood Ca, P, and sugar levels, as well as fluoride levels and ash contents in teeth and bone, and fat glycogen, and fluoride levels in the liver. Fed to men exposed to elevated fluoride uptakes, 100mg of Vitamin C increased the excretion of fluoride from 3-5.5 mg/day to 6-8.5 mg/day (17).

Most important, however, are the following findings:

1.) in guinea pig, fluoride added to the diet cannot make teeth more insoluble (caries-resistant) than the addition of Vitamin C to the diet and-

2.)  in low fluoride areas, dietary supplementation with Vitamin C leads to fluoride deposition in teeth equal to the of higher fluoride areas (18, 19).

In conclusion, it appears that Vitamin C is and essential factor in the deposition of fluoride in, as well as the exclusion of fluoride from, various tissues in the body.

While increased fluoride in teeth had been correlated to caries-resistant of teeth, adequate Vitamin C levels in the diet in areas of 0.1 to 0.5 ppm fluoride (and even 0.01 to 0.05 ppm in the nursing infant) leads to adequate uptake by the teeth. Indeed in animals that manufacture there own Vitamin C (e.g. rats), Fluoride is found not to have a caries protective effect until it reaches levels of 10-20 ppm (14); at these levels it acts as a strong antibacterial in the mouth.

The indiscriminate fluoridation of water systems is not the solution to the problems of tooth decay. In the absence of sufficient Vitamin C, fluoridation will lead to Vitamin C depletion, dental fluorosis, and to abnormal levels of metabolites in blood tissues.

Adequate intake of Vitamin C may explain why people or populations in low fluoride areas can be caries-free.

REFERENCES:

(1)           Y. Ericsson, U. Ribelius, Caries Research 5, 78 (1971);

(2)           F.J. McClure, Personal communication.

(3)           A. Sheiham, British Dental Journal 123, 144 (1967;

(4)           J.P. Quinn, NDRI-PR-68-03, (June 1968) 11pp. US Nat.Tech.   Inf. Serv.
                 Reo. No. AD0839 129;

(5)           S.J. Barnaud Journal 2, Med. Trop. 29, 593 (1969);

(6)           J.A. Cran, Australian Dental Journal 2, 277 (1957);

(7)           F. Prader, Schweiz. Mschr. Zahnhk. 71 885 (1961);

(8)           R.S. Nanda, Indian Journal of Dental Research 60, 1470 (1972);

(9)           Y. Imai, Koku Eisei Gakkai Zasshi 22, 144 (1972);

(10)          P.H. Phillips, J. Biol. Chem. 100, (Proc. Am. Soc. Biol. Chem. 8)
               Lxxix (1933);

(11)          P.H. Phillips, F.J. Stare, C.A. Elvenhem, J. Biol. Chem. 106, 41 (1934);

(12)          N.A. Ivanova, Voprosy Okhrany Materinstva I Detstva 4, 29 (1959);

(13)          F.F.V. Atkinson, G.C. Hard, Nature 211, 429 (1966);

(14)          N.M. Stiles, National Institute Of Dental Research,

Personal Communication;

(15)          J.W. Suttie, P.H. Phillips, The Pharmacology and Toxicology of Fluorine,

                   J.C. Muhler, M.K. Hine, Ed.  (Bloomington, Indiana University Press, 1959) pp 70-7;

(16)          V.S. Andreeva Voprosy Okhrany Materinstva I Detstva 4, 25 (1959);

(17)          R.D. Gabovich, P.N. Maistruck, Voprosy Pitaniya 22, 32 (1963);

(18)          D. J. Thompson, P. H. Phillips, J. Dent. Res. 45, 845 (1966);

(19)          D. Triers, C.G. Elliott, M.D. Smith, J. K. Dent. Res. 47, 1171 (1968);

(20)          W. Buttner, Advances in fluorine Research and Dental Caries Prevention,

                   J. L. Hardwick, H.R.Held, K.G. Konig, Ed.

(New York Pergamon Press, 1965) pp. 19-30;

Yiamouyiannis was so effective in writing and debating his point of view, that American Dental organizations advised their members not to engage this man in conversation about fluoride.

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VITAMIN C REDUCTION OF F. INDUCED
 EMBRO-TOXICITY IN RATS

Department of Zoology,
University School of Sciences,
Gujarat University,
Ahmedabad 380 009, India
R J Verma, D M Guna Sherlin
Jai Research Foundation, Vapi, Valvada 396 108, India

Oral administration of sodium fluoride (40 mg/kg body weight)from day 6 to 19 of gestation caused, as comparedto control, significant reductions in body weight, feed consumption, absolute uterine weight and numberof implantations. Significantly higher incidenceof skeletal (wavy ribs, 14th rib, <6 sternal centre, dumbell-shaped second and fifth sternebrae, incompleteossification of skull and thickening of tibia)and visceral (subcutaneous haemorrhage) abnormalities were alsoobserved in NaF-treated dams than that of control.Oral administration of vitamin C (50 mg/kg bodyweight) and vitamin E (2 mg/0.2 ml olive oil/animal/day) fromday 6 to 19 of gestation along with NaF significantlyameliorates NaF-induced reductions in body weight,feed consumption, absolute uterine weight (only with vitaminE treatment) and number of implantations. Ascompared with NaF-treated alone, the total percentageof skeletal and visceral abnormalities were significantly loweredin fluoride plus vitamin C-treated animals.Vitamin E was less effective.

These findings suggest that vitamin C significantly reduced the severity andincidence of
fluoride-induced embryotoxicity in rats.
Key Words:
fluoride • vitamins • embryotoxicity • amelioration

Human & Experimental Toxicology, Vol. 20, No. 12, 619-623 (2001)

Our comment:
Unlike humans and guinea pigs rats and most animals
manufacture vitamin C in their livers.

FLUORIDE LINKED TO PRE-TERM
BIRTH & ANEMIA IN PREGNANCY

Study Links Fluoride To Pre-term Birth And Anemia In PregnancyMain Category: Pregnancy / ObstetricsAlso Included In: Blood / Hematology; Pediatrics / Children’s Health; Nutrition / DietArticle

Date:  03 Sep 2010 – 2:00 PDT

Fluoride avoidance reduced anemia in pregnant women, decreased pre-term births and enhanced babies’ birth-weight, concludes leading fluoride expert, A K Susheela and colleagues, in a study published in Current Science (May 2010).

Susheela’s team explains that anemia in pregnancy, which can lead to maternal and infant mortality, continues to plague many countries despite nutritional counseling and maternal iron and folic acid supplementation. This is the first examination of fluoride as an additional risk factor for anemia and low-birth-weight babies.

Anemic pregnant women living in India, whose urine contained 1 mg/L fluoride or more, were separated into two groups. The experimental group avoided fluoride in water, food and other sources and ate a nutritious diet per instruction. The control group received no instructions. Both groups supplemented with iron and folic acid.

Results reveal that anemia was reduced and pre-term and low-birth-weight babies were considerably fewer in the fluoride-avoidance group as compared to the control. Two stillbirths occurred in the control group, none in the experimental group.

Susheela et al. writes, “Maternal and child under-nutrition and anemia is not necessarily due to insufficient food intake but because of the derangement of nutrient absorption due to damage caused to GI (gastrointestinal) mucosa by ingestion of undesired chemical substances, viz. fluoride through food, water and other sources.”

Fluoride avoidance regenerated the intestinal lining which enhanced the absorption of nutrients as evidenced by the reduction in urinary fluoride followed by rise in hemoglobin levels, they report.

Could the same thing be happening in the United States? State University of New York researchers found more premature births in fluoridated than non-fluoridated upstate New York communities, according to a presentation made at the 2009 American Public Health Association’s annual meeting.

Current Science reports that adverse reactions of fluoride consumption are known to occur including reducing red blood cells, reducing blood folic acid activity, inhibiting vitamin B12 production and the non-absorption of nutrients for hemoglobin biosynthesis.

“Citizens must demand that water fluoridation be stopped,” says attorney Paul Beeber, President, New York State Coalition Opposed to Fluoridation, Inc. “It’s disturbing that public-health officials and organized dentistry continue to ignore the overwhelming evidence revealing fluoride to be non-nutritive, unnecessary and unsafe,” says Beeber.

Source: NYS Coalition Opposed to Fluoridation, Inc.

Fluoride will undoubtedly continue to be ignored,
because the masterminds behind its marketing
are still claiming after over a half a century of
unproven experimentation that it is good for us.

More on Vitamin C Deficiency and Fluoride
It is also worth noting the link between fluoride and other micronutrients;
in particular Vitamin C. Vitamin C is an essential nutrient for humans
and is required by the body to form collagen in bones,
cartilage, muscle and blood vessels. It also aids in
the absorption of iron.[449]

It has been documented that in the absence of sufficient Vitamin C, water fluoridation will lead to Vitamin C depletion, dental fluorosis and to abnormal levels of metabolites in blood tissues.[450] Animal studies have also demonstrated the link between Vitamin C and fluoride intake.[451] The findings of this latter study support the previous observations noted by Yiamouyiannis. This fact should be of particular interest to the Irish health authority as a national health survey has documented the inadequacy of Vitamin C intake in boys and girls aged from 5 to 12 years in Ireland.[452] A more recent study among adults aged 65 years and over, similarly showed a low intake of Vitamin C in addition to inadequate intakes of calcium, Vitamin A and Vitamin D.[453]

Alarmingly, it is possible that water fluoridation may itself be contributing to Vitamin C depletion as well as dental fluorosis in Ireland. Interestingly, it has also been observed that in low fluoride areas, dietary supplementation with Vitamin C leads to fluoride deposition in teeth equal to that of higher fluoride areas with water fluoridation.[454],[455] It is plausible therefore, to assume, that exposure to fluoride compounds in drinking water may increase the associated risk of  Vitamin C depletion, a contributory factor associated in the development of both dental fluorosis and periodontal disease.

Indeed the coexistence of fluorosis and signs of Vitamin C deficiency have been reported[456],[457] and it has been suggested that low concentrations of  Vitamins A, C and D tend to worsen the symptoms of fluorosis and accelerate the development of fluoride toxicosis.[458]

 Footnotes    (↵ returns to text)

1. 449 Mayo Foundation for Medical Education and Research↵2. 450 Vitamin C and Fluoridation- John A. Yiamouyiannis Ph.D.↵

3. 451 Verma RJ, Sherlin DM , Fluoride and Vitamin C, Human & Experimental Toxicology, 2001 Dec;20(12):619-23.↵

4. 452 Irish Universities Nutrition Alliance (IUNA), 2001, Adequacy of micronutrient Intakes in Ireland, Results from the National Food Consumption Surveys,↵

5. 453 Irish Universities Nutrition alliance (2008), National Teens Food Survey↵

6. 454 D. J. Thompson, P. H. Phillips, Journal of Dental Research. 45, 845 (1966).↵

7. 455 D. Triers, C.G. Elliott, M.D. Smith, J. K. Dent. Res. 47, 1171 (1968).↵

8. 456 Krishnamachari K. A. V. R, and Laxmaiah N., Lack of effect of massive dose of vitamin C on fluoride excretion in fluorosis during a short clinical trial,
The American Journal of Clinical Nutrition 28: November 1975, pp. 1234-1236.↵

9. 457 Pandit, C. G., I. N. S. Raghavachari, D. S. Rao And V. Krishnamurthy. Endemic fluorosis in South India. A study of the factors involved in the production of mottled anamel in children and severe bone manifestations in adults. Indian J. Med. Res. 28: 559, 1940.↵

458 Suttie JW, Phillips PH: Fluoride ingestion and vitamin metabolism. In Fluorine and Dental Health: the Pharmacology and Toxicology of Fluorine. JC Muhler and MK Hine eds.

BloomingtonI, N: Indiana University Press, 1959, pp 70-77.↵

SEE ALSO ↓

Vitamin C – Stone-Pauling-Kalokerinous & Ebola

 Vitamin C Foundation

…Then I happened across a report on fluoride and it’s negative effect
on collagen synthesis. I immediately switched to water without fluoride
and the results were magical. This may be unique to my chemistry.
But given the volume of research, it might be worth recommending…

— FLUOROSIS —

COAL BURNING  –  CHINA

106 Fluoride Vol. 36 No. 2 106-112 2003 Research Report

For Correspondence:
Prof Wuyi Wang, Institute of Geographical Sciences & Natural
Resources Research, Chinese Academy of Sciences,
Beijing 100101, China.
E-mail: wangwy@igsnrr.ac.cn

ENVIRONMENTAL EPIDEMIC CHARACTERISTICS

OF COAL BURNING ENDEMIC FLUOROSIS AND

THE SAFETY THRESHOLD OF COAL FLUORIDE IN CHINA

Yonghua Li, Wuyi Wang, a Linsheng Yang, Hairong Li

Beijing, China

SUMMARY:  Data on coal-burning endemic fluorosis throughout China and on the exposure-response relationship between concentrations of fluoride determined in coal samples and the prevalence of dental fluorosis reported from 17 representative surveillance stations in Southwest China were used to estimate the safety threshold for coal fluoride. Coal-burning endemic fluorosis occurs mainly in the mountainous areas of this part of China, where the prevalence of the disease is closely linked to geochemical parameters of the local environment. In these regions the incidence of dental fluorosis has a significant positive correlation with the concentration of fluoride in coal. The safety threshold of coal fluoride is estimated to be 190 mg/kg by the criterion of 0% incidence of dental fluorosis.

Keywords: China; Coal fluoride; Endemic fluorosis; Safety threshold.

INTRODUCTION

Fluorine (F), the most electronegative and reactive of the halogens, is a common chemical element in the earth’s crust in combined form. F concentrations in rocks and soils are well documented, but data on the F concentration in coal are relatively limited.

1-4 Swaine reported the total F concentration in coal ranges from 20 to 500 mg/kg.

5  Statistical data indicate that the mean concentration of F in coal worldwide is 80 mg/kg, but in China it is 200 mg/kg.

6 In the mountainous areas of Southwest China, it is even higher— up to 3106 mg/kg in local coal.

7  Fluoride in coal can be released into the ambient environment as atmospheric F, waterborne F, and residue F during mining, handling, and combustion.

6-8 In Southwest China, F

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PATENTS ON FLUORIDE RAT POISON

& INSECTICIDES

rat cocy mozy

© Peter Meiers

From the “Introduction” to Chapter 7, “Fluorine-containing insecticides”,
by R. L. Metcalf (Handb. exp. Pharmacol. XX.1, pp. 355-386, Springer,
Berlin-Heidelberg-New York, 1966):

“Fluorine has played a significant role in insect control since about 1896 when sodium fluoride and various iron fluorides were patented in England as insecticides. Sodium fluoride was used in the United States for cockroach control before 1900 and was introduced in 1915 for the control of poultry lice. However, the use of fluorine insecticides did not become general until the 1930´s when the disadvantages of arsenical residues on food crops became apparent and the inorganic fluorine compounds were introduced as safer substitutes. Systematic investigation of organofluorine insecticides began about 1935 in the I. G. Farbenindustrie and the fluoroalcohols and fluorophosphates (phosphorofluoridates) were intensively investigated largely through the research of Schrader (1952). During World War II fluoro-DDT or “Gix” was used for the control of insects of medical importance. More recently, fluoroacetamide and analogues have been used as systemic insecticides and a large variety of other fluorinated organic compounds have shown insecticidal activity. Sulfuryl fluoride has recently been marketed as a fumigant for household and structural pests…”

Alvord and Dietz, of Grasselli Chemical Company, Cleveland, Ohio, point out certain problems with the use of soluble fluorides as insecticides (Ind. Eng. Chem. 25 (June 1933) 629-633):

“The fact that sodium fluoride would control certain types of insects had been known for many years, but all attempts to use it and other fluorine compounds on plants failed because of plant injury. Progress along the line of utilizing the fluorine compounds in this connection really began with the discovery by Roark that the relatively insoluble fluorides would not injure the foliage and would control certain insects. About the time of this discovery, the Grasselli Chemical Company began to experiment with barium fluosilicate. The development of this material was held back for several years because of plant injury following its use, and it was not until the discovery, quite by accident, that the injury was due to an unsuspected impurity and that the pure compound was in reality safe to most foliage, that rapid progress was made.”

S. Marcovitch gives some details as to how those fluoride insecticides  work (Ind. Eng. Chem. 16 (1924) 1249):

“The value of sodium fluosilicate as an insecticide is due to the fact that it is both a contact and stomach poison. Shafer has determined that when a roach walks over powdered sodium fluoride a little of the powder adheres to the lower part of the body, antennae and tarsi of the feet, and dissolves in the exudations of the integument. This seems to cause some irritation and uneasiness; the insect soon begins to clean the moistened powder from the body by licking it. In doing this enough of the poison may be brought into the mouth and swallowed, to kill after a period varying in from five to ten days. Other insects, such as Mexican bean beetles, also have the habit of cleaning themselves and by putting their feet in their mouths become very easy to kill. For this reason the sodium fluosilicate is more effective against the adult beetles than the larvae, which do not have these habits.”

Because of such habits, toxicity to higher animals became of concern (Marcovitch S.: “The fluosilicates as insecticides”, Ind. Eng. Chem. 18 (June 1926) 572-573

The Patents:

1896

Charles Henry HIGBEE, of New York City, N.Y., Manager of Manufacturing Company: “An improved composition or material for destroying insects”, British Patent GB 8236; filed April 18, 1896; pat. May 23, 1896. (“The compounds of fluorine which I employ for the purpose of destroying insects, are certain soluble ones, viz.: sodium fluoride, ferric fluoride, the silico-fluorides of the same bases, hydro-fluo-silicic acid, and the boro-fluo-silicates”, which the inventor claims to be less toxic for humans then many of the compounds then in use for the same purpose, i.e. “arsenic, copper, phosphorus, and the like”)

1906

Karl Heinrich WOLMAN and Bernard DIAMAND, Idaweiche, Oberschlesien, Germany, assignors to Max Marschall, Nice-Cimiez, France: “Preserving composition for fibrous material”, US Patent 934,871; filed Nov. 6, 1906; granted Sept. 21, 1909  (uses “sodium fluorid” and “sodium silico-fluorid”. “We have also found that the salts of hydrofluoric acid and of silicofluoric acid both of which are weak, bactericidal acids when used in connection wioth a strong mineral acid, as above set forth, will produce good results …”)

1908

Carleton ELLIS, assignor, by mesne assignments, to Chadeloid Chemical Company, of New York, N.Y.: “Insecticide”, US Patent 1,082,507; filed March 11, 1908; pat. Dec. 30, 1913 (“The composition comprises a solution of wax in carbon bisulfid, or similar penetrating organic liquid, emulsified with an aqueous solution, considerably thickened for the purpose of emulsification, and carrying in solution a powerful insecticide such as inorganic compounds like bichlorid of mercury and ammonium fluorid, or organic compounds like ammonium formate, etc.”)

1911

Jacques WITTLIN, of Vienna, Austria-Hungary, assignor of one-half to Siegfried Schlewinger, of New York: “Antiseptic”, US Patent 1,044,840; filed Jan. 12, 1911; granted Nov. 19, 1912 (“… my present invention further contemplates the incorporation of ammonium fluorid or equivalent fluorin-containing salts or fluorin compounds in the preparation of the antiseptic, whereby the germicidal or disinfectant properties thereof are very materially increased.”)

1921

Henry Edward Percy HUTCHINGS, of Barking Essex, UK: “Improvements in or relating to rat and other vermin poisons”, British Patent GB 187,424; filed Sept. 15, 1921; pat. Oct. 26, 1922  (a bait for the purpose of rat and mouse extermination, with additions of either sodium fluoride, barium carbonate, squill or oxalic acid, to serve as a basic poison)

1923

Rurik C. ROARK, Baltimore, Md.: “Insecticide”, US Patent 1,524,884; filed Aug. 6, 1923; granted Feb. 3, 1925 (“The poisonous action of soluble fluorides is well known and has been utilized for the control of injurious insects. For example, sodium fluoride, a salt readily soluble in water, is a very effective roach poison and is a common ingredient of roach powders. Potassium and barium fluorides have been similarly employed …”)

“There is nothing new in the use of sodium fluosilicate as an insecticide. Its use for that purpose was described nearly thirty years ago by HIGBEE (English Patent No. 8236, May 23, 1896). More recently, WILLE has reported tests with sodium fluosilicate against roaches and COBENZL mentions it as a common ingredient of rat and insect poisons” (Roark C., Department of Agriculture: “Fluorides vs. fluosilicates as insecticides”, Science 63 (April 23, 1926) 431-2)

1926

Bernard GEHAUF and Harold W. WALKER, of Edgewood, Md.: “Method of making silicofluorides and products thereof”, US Patent 1,617,708; filed May 14, 1926; pat. Feb. 15,1927 (“This invention … also comprises a new composition of matter for insecticidal and other purposes … made by neutralizing hydrofluosilicic acid with the appropriate base … Hydrofluosilicic acid ordinarily is prepared by contacting various waste gases containing silicon fluorid with water.. Waste gases containing silicon fluorid arise in various industries, as in the manufacture of superphosphates.”)

Martin J. FORSELL, Seattle, Washington: “Insecticide”, US Patent 1,618,702; filed Aug. 30, 1926; granted Feb. 22, 1927 (“The insecticide consists of using apple after it is dried and powdered and mixing therewith any well-known poison in powdered form … any one of the compounds of fluorine preferably sodium or potassium fluoride or sodium or potassium silico fluoride …)

Howard S. McQUAID, Cleveland, Ohio, assignor to The Grasselli Chemical Company, of Cleveland, Ohio: “Production of Barium Silicofluoride”; US Patent 1,648,143; filed Nov. 22, 1926; patented Nov. 8, 1927 (Process for production of barium silicofluoride from sodium silicofluoride for use as an insecticide)

1927

Hermann STÖTTER, Leverkusen, assignor to I.G. Farbenindustrie Akt.-Ges., Frankfurt a. M.: “Verfahren zum Schützen von Wolle, Pelzwerk u. dgl. gegen Mottenfraß”, German Patent (DE) 485,101; filed May 26, 1927; granted Oct. 10, 1929  (ammonium bifluoride, potassium ammonium fluoride)

1929

Roscoe H. CARTER, Washington D.C. (Government employee): “Process for the manufacture of insecticides and method of making same”, US Patent 1,842,443; filed Nov. 15, 1929; granted Jan. 26, 1932  (“As pointed out in other patent applications of mine, the double fluorides of the alkali metals are useful insecticidal materials and can be formed from water soluble salts of aluminum by treatment with alkali metal compounds and fluorine acids in the proper molecular proportions.”)

1931

Arthur H. HENNINGER, assignor to General Chemical Company, New York: “Process of making potassium aluminum fluoride”, US Patent 1,937,956; filed June 18, 1931; pat. Dec. 5, 1933 (“… for use as an insecticide. It has heretofore been proposed to use potassium aluminum fluoride as an insecticide for the control of various insect pests. This material is considered to possess advantages over lead arsenate as an insecticide for the reason that, although poisonous, the fluoride compound is less toxic to human beings and animals than is lead arsenate.”)

1932

Earl B. ALVORD, assignor to Grasselli Chemical Company, Cleveland, Ohio: “Noncorrosive insecticdal compositions”, US Patent 1,931,367; filed Aug. 24, 1932; patented Oct. 17, 1933 (addition to their barium fluosilicate of a slightly water-soluble substantially neutral fluoride (such as cryolite, or barium fluoride) to overcome corrosive effects of the barium fluosilicate upon spray pumps)

1938

John E. MORROW, assignor to Aluminum Company of America: “Insecticide and method of producing same”, US Patent 2,210,594; filed Jan. 6, 1938; pat. Aug. 6, 1940 (“Double fluorides of sodium and aluminum, such as natural and synthetic cryolite, have been used as insecticides, and the usefulness of such compounds as stomach poisons for various insects has been established. It has been demonstrated, for example, that these fluorides are particularly useful in combatting the codling moth and the Mexican bean beetle.”)

1948

Alan BELL, Kingsport, Tennessee, assignor to Eastman Kodak Company, Rochester, N. Y.: “Insecticidal compositions comprising either hexyl alkyl tetraphosphate or tetra-alkyl pyrophosphate and either an alkali metal fluoride or fluorosilicate”, US Patent 2,514,621; filed Dec. 26, 1948; granted July 11, 1950  (“Diethyl phosphate is the hydrolysis product produced by most of these phosphorus insecticides such as organic insecticides derived from triethyl phosphate – thionyl chloride reaction product, hexaethyltetraphosphate, tetraethylpyrophosphate. This hydrolysis product is not as toxic as parent compound in itself but mixed with NaF or Na2SiF6 has considerable toxicity.”)

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“FLUORIDES, THE DEADLY TOXIN WITHIN”

Abdul Razak

Professor Dzulkifli Abdul Razak

National Poison Centre
Universitiy Sains Malaysia -
2 September 2001

Following the recent withdrawal of the cholesterol-lowering drug Lipobay, there is now a new perspective to the issue, the drug being a fluoride-containing compound. The drug, also known by its generic name, cerivastatin, is one of the many such compounds pulled off the shelves in the last few years.

Cerivastatin was taken off because of at least 40 deaths worldwide, 31 in the US alone. According to a recently released commentary by a Canadian group, Parents of Fluoride Poisoned Children, a series of fluoride containing drugs or so-called fluorinated drugs have been withdrawn from the market in the last 10 years due to their toxic effects on human beings. One notable example is the combination “Fen-Phen” (a generic combination of fenfluramine and phentermine, the former being a fluorinated drug type) which was said to have weight-reducing effects. Others are dexfenfluramine (Redux) and fenfluramine (Pondimin).

There are at least eight other examples of fluorinated drugs withdrawn so far, because serious side effects on the heart, and for suspected adverse influence on thyroid hormone activity.

They include, last year, cisapride (Propulsid) because of its severe side-effects on the heart. In 1999, two drugs were withdrawn.

These were an anti-allergy drug, astemizole (Hismanal); and grepafloxacin (an antibiotic, Raxar) because they too were associated with similar adverse events.

In 1998, patients with congestive heart failure using the drug mibedrafil (Posicor) showed a trend to higher mortality, causing it to be withdrawn.

Alredase (Tolrestat, an anti-diabetic) was withdrawn in 1997 after the appearance of severe liver toxicity and deaths among several patients. In the same year too fenfluramine (part of Fen-Phen) and dexfenfluramine were withdrawn.

In 1993, flosequinan (Manoplax, a heart drug) was withdrawn when it was shown that the beneficial effects on the symptoms of heart failure did not last beyond the first three months of therapy. After that, patients had a higher rate of hospitalization than patients taking a placebo.

Of the many fluorinated drugs that remain in the market some carry warnings of serious cardiac toxicity, for instance halofantrine, a schizonticidal drug. More specifically, other fluorinated drugs, although they have not yet been withdrawn, are known to cause muscle wasting or rhabdomyolysis; like cerivastatin.

For instance, the PFPC commentary noted that the fluorinated antibiotic fluoroquinolone, used to treat infections, is reported to cause tendonitis and rhabdomyolysis. In fact product information for such antibiotics (enoxacin, fleroxacin, norfloxacin, sparfloxacin, and tosufloxacin) was amended in Japan in October 1994, to state that rhabdomyolysis may occur. Reportedly, the tragic story involving fluorinated drugs (the fluorophenyls in particular, initially limited to industrial use involving dyes and pesticides) can be traced way back to the 1930s when they were used to treat hyperthyroidism.

The use followed a discovery by IG Farben (Bayer) and Knoll’s scientists that all fluoride compounds can interfere with thyroid hormone activity.

In the liver especially, organic fluoride compounds undergo extensive transformation, mainly via oxidative demethylation, involving the thyroid hormone (T3) mediated P-450 enzyme system. And the resulting metabolites may have higher activity and/or greater toxicity than the original compound.

The activity of organic fluoride compounds on the P-450 enzyme system is critical as it relates to the elimination of many other drugs. Inhibition of these enzymes can cause other drugs to accumulate to dangerous levels in the body, leading to hazardous drug interactions. In many cases fluorinated drugs are being implicated as documented in hundreds of well-established studies.

Moreover, adds PFPC, the metabolites produced by organic fluoride compounds in the liver can be transferred to the fetus through various pathways, including circulatory via placental passage, gastrointestinal via fetal swallowing, and respiratory secondary to fetal lung absorption. This may lead to congenital abnormalities as in the case of fluconsazole (Diflucan).

In short, going by the above evidence, fluorinated drugs seem to pose a number of risks associated with the fluorine or fluoride contained in them. It raises even more concern when fluoride itself is present in many industries and products, including food and drinks, without any rigorous evaluation or monitoring.

Of late, we have managed to label all toothpastes containing fluoride in this country. But this is clearly a minuscule effort in the attempt to regulate the use of fluoride as an inherent poison. We need to do more now.

For more information, contact the National Poison Centre at Universiti Sains Malaysia,

tel: 04-657 0099, fax: 04-656 8417, Update 

Source: New Sunday Times (Focus) September 2, 2001

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The ability of fluoride to reduce thyroid hormone levels has been know for over 100 years (Maumene 1855).

The Social Implications of Neuroscience:

Linking Brain Biochemistry and Violent Crime

Roger D. Masters (Dartmouth College)·

THIS FILE IS A DRAFT OF THE CHAPTER WITH THIS TITLE

Richard W. Bloom and Nancy Dess, eds.,
Evolutionary Psychology and Violence:

rodger-d-master-f

A Primer for Policymakers and Public Policy Advocates
(Westport: Praeger, 2003), pp. 23-56.

ABSTRACT:

It is impossible to deny that a revolution in neuroscience and other areas of biology has taken place over the last half-century.  The  estimates of 83 million Americans taking drugs like Prozac for depression and 11 million children on Ritalin for hyperactivity indicate it is time to reconsider the role of brain chemistry in social behavior and violent behavior.  Since it is obvious that loss of impulse control can contribute to violent outbursts – and evidence shows that some toxic chemicals (such as lead) can have this effect, it is time to consider neuroscientific evidence linking environmental toxins and rates of violent behavior.  To illustrate the implications of the new issues involved, I focus on a hitherto unexplored example.  Two chemicals (H2SiF6 and Na2SiF6, jointly called “silicofluorides” or SiFs) are used to treat public water supplies of 140 million Americans even though, as the EPA has admitted, they never been tested for safety.  To illustrate the interdisciplinary complexities entailed when linking brain chemistry to policy decisions concerning violent crime, our argument has four main stages: first, why might SiFs be dangerous? Second, what biochemical effects of SiF could have toxic consequences for humans?  Third, on this basis a research hypothesis is formulated to measure the types of harm.  In this case, we predict children in communities using SiF should have increased uptake of lead from environmental sources and higher rates of behavioral dysfunctions such as hyperactivity (ADHD) known to be caused by lead neurotoxicity.  Finally, the hypothesis is tested using multiple sources of data including rates of violent crime studied using a variety of multivariate statistical techniques (including analysis of variance, multiple regression, and stepwise regression).  As this outline should make clear, a combination of interdisciplinary perspectives and great prudence is needed to link research in neuroscience to policies concerning violent crime,  If confirmed, however, the potential benefits of hypotheses like the one tested below may be great, revealing the generally unsuspected value of including neuroscientific research in the analysis of human social behavior.

Requests for reprints and correspondence should be directed to: Prof. Roger D. Masters, Department of Government, HB 6222, Dartmouth College, Hanover, NH 03755. Email: Roger.D.Masters@Dartmouth.edu

The full version of the above is on the net,
and as the above suggests adding silicofluorides
to drinking water amounts to domestic terrorism.

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ukrainian-cretin-farm-women

MF-Cretins-f

Image of 3 Cretins

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THE RELATIONSHIP OF A LOW-IODINE AND
HIGH-FLUORIDE ENVIRONMENT TO
SUBCLINICAL
CRETINISM* IN XINJIANG (China)

by

Lin Fa-Fu, Aihaiti, Zhao Hong-Xin,
Lin Jin, Jiang Ji-Yong, Maimaiti, and Aiken.

Extract:

… Xinjiang Institute for Endemic Disease Control and Research;

Office of Leading Group for Endemic Disease Control

of Hetian Prefectural

Committee of the Communist Party of China; and County Health

and Epidemic Prevention Station, Yutian, Xinjiang.

Cretinism in iodine-deficiency areas is well known, yet the milder forms of somatic and psychomotor maldevelopment and thyroid dysfunction caused by iodine deficiency may be more difficult to detect. DeQuervain, in 1936, called this milder form “semi-cretinism,” while in 1980 Laggasse used the term “cretinoidism.” It was formally named “subclinical endemic cretinism” at a symposium on subclinical cretinism held in Xinzhou, Shanxi province in 1985.

Currently, attention is being focused on these disorders in China and abroad. The Hetian prefecture in Xinjiang has reportedly been one of the Asian areas most severely affected by iodine deficiency disorders (IDD).

During the period 1987-1989, we made a systematic survey of subclinical endemic cretinism in this district under a UNICEF aid Project.

Materials and Methods

General conditions and selection of affected areas – The entire region of Xinjiang in central Eurasia is affected by iodine deficiency. The study area, located between the southern border of Tarim basin and the northern slope of Kunlun Mountains, is arid with sandy soil and an annual precipitation less than 50 mm. The cultivated alluvial plain extends from south to north with a steepening gradient. The geographical distributions of endemic goiter and endemic fluorosis are characterized by marked vertical zones. The inhabitants are of lower socioeconomic status, with an annual mean income of about 200 yuan (RMB) per person.

Area with high fluoride and low iodine levels (Area A) – In the township Xinyuan in the lower reaches of Kliya river in the county of Yutian, north of the highway, we examined 250 schoolchildren, aged 7-14 years. The goiter prevalence was 91% and dental fluorosis 20.80%. The average level of iodine in drinking water was 5.21 mg/l, and that of fluoride 0.88 mg/l.

Area with low iodine level (area B) – In the townships of Langan and Jiayi in the alluvial plain before the mountains and to the south of the highway, we examined 256 schoolchildren, aged 7-14 years. The goiter prevalence was 82% and dental fluorosis of 16.00%. The average water iodine level was 0.96 mg/l and that of fluoride 0.34 mg/l. …

CRETINISM is the condition wherein the child has severely stunted physical growth due to untreated congenital iodine deficiency while myxedema is a form or cutaneous and dermal edema due to increased deposition of the connective tissue components. The subcutaneous tissues are seen in hypothyroidism and Grave’s disease.

Reports of this problem are surfacing in parts of Australia where
water fluoridation has been operating for many years!

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Barry Durrant-Peatfield

THE EFFECTS OF FLUORIDE ON THE THYROID GLAND
by
Dr Barry Durrant-Peatfield MBBS LRCP MRCS,

There is a daunting amount of research studies showing that the widely acclaimed benefits on fluoride dental health are more imagined than real. My main concern however, is the effect of sustained fluoride intake on general health. Again, there is a huge body of research literature on this subject, freely available and in the public domain.

But this body of work was not considered by the York Review when their remit was changed from “Studies of the effects of fluoride on health” to “Studies on the effects of fluoridated water on health.” It is clearly evident that it was not considered by the BMA (British Medical Association), British Dental Association (BDA), BFS (British Fluoridation Society) and FPHM, (Faculty for Public Health and Medicine) since they all insist, as in the briefing paper to Members of Parliament – that fluoridation is safe and non-injurious to health.

This is a public disgrace. I will now show by reviewing the damaging effects of fluoridation  with special reference to thyroid illness.

It has been known since the latter part of the 19th century that certain communities, notably in Argentina, India and Turkey were chronically ill, with premature ageing, arthritis, mental retardation, and infertility; and high levels of natural fluorides in the water were responsible. Not only was it clear that the fluoride was having a general effect on the health of the community, but in the early 1920s Goldemberg, working in Argentina showed that fluoride was displacing iodine; thus compounding the damage and rendering the community also hypothyroid from iodine deficiency.

‘HIGHLY DAMAGING TO THE THROID GLAND’

This was the basis of the research in the 1930s of May, Litzka, Gorlitzer von Mundy, who used fluoride preparations to treat over-active thyroid illness. Their patients either drank fluoridated water, swallowed fluoride pills or were bathed in fluoridated bath water; and their thyroid function was as a result, greatly depressed. The use in 1937 of fluorotyrosine for this purpose showed how effective this treatment was; but the effectiveness was difficult to predict and many patients suffered total thyroid loss. So it was given a new role and received a new name, Pardinon. It was marketed not for over-active thyroid disease but as a pesticide. (Note the manufacturer of fluorotyrosine was IG Farben who also made sarin, a gas used in World War II).

This bit of history illustrates the fact that fluorides are dangerous in general and in particular highly damaging to the thyroid gland, a matter to which I shall return shortly. While it is unlikely that it will be disputed that fluorides are toxic – let us be reminded that they are Schedule 2 Poisons under the Poisons Act 1972, the matter in dispute is the level of toxicity attributable to given amounts; in today’s context the degree of damage caused by given concentrations in the water supply. While admitting its toxicity, proponents rely on the fact that it is diluted and therefore, it is claimed, unlikely to have deleterious effects.

THEY COULD NOT BE MORE MISTAKEN…

It seems to me that we must be aware of how fluoride does its damage. It is an enzyme poison. Enzymes are complex protein compounds that vastly speed up biological chemical reactions while themselves remaining unchanged. As we speak, there occurs in all of us a vast multitude of these reactions to maintain life and produce the energy to sustain it. The chains of amino acids that make up these complex proteins are linked by simple compounds called amides; and it is with these that the fluorine molecules react, splitting and distorting them, thus damaging the enzymes and their activity. Let it be said at once, this effect can occur at extraordinary low concentrations; even lower than the one part per million which is the dilution proposed for fluoridation in our water supply.

THE BODY CAN ONLY ELIMINATE HALF OF THE TOTAL INTAKE

Moreover, fluorides are cumulative and build up steadily with ingestion of fluoride from all sources, which include not just water but the air we breathe and the food we eat. The use of fluoride toothpaste in dental hygiene and the coating of teeth are further sources of substantial levels of fluoride intake. The body can only eliminate half of the total intake, which means that the older you are the more fluoride will have accumulated in your body. Inevitably this means the ageing population is particularly targeted. And even worse for the very young there is a major element of risk in baby formula made with fluoridated water. The extreme sensitivity of the very young to fluoride toxicity makes this unacceptable. Since there are so many sources of fluoride in our everyday living, it will prove impossible to maintain an average level of 1ppm as is suggested.

WHAT IS THE RESULT OF THESE TOXIC EFFECTS?

First the immune system. The distortion of protein structure causes the immune proteins to fail to recognize body proteins, and so instigate an attack on them, which is Autoimmune Disease. Autoimmune diseases constitute a body of disease processes troubling many thousands of people: Rheumatoid Arthritis, Systemic Lupus Erythematosis, Asthma and Systemic Sclerosis are examples; but in my particular context today, thyroid antibodies will be produced which will cause Thyroiditis resulting in the common hypothyroid disease, Hashimoto’s Disease and the hyperthyroidism of Graves’ Disease.

Musculo Skeletal damage results further from the enzyme toxic effect; the collagen tissue of which muscles, tendons, ligaments and bones are made, is damaged. Rheumatoid illness, osteoporosis and deformation of bones inevitably follow. This toxic effect extends to the ameloblasts making tooth enamel, which is consequently weakened and then made brittle; and its visible appearance is, of course, dental fluorosis.

The enzyme poison effect extends to our genes; DNA cannot repair itself, and chromosomes are damaged. Work at the University of Missouri showed genital damage, targeting ovaries and testes. Also affected is inter uterine growth and development of the foetus, especially the nervous system. Increased incidence of Down’s Syndrome has been documented.

Fluorides are mutagenic. That is, they can cause the uncontrolled proliferation of cells we call cancer. This applies to cancer anywhere in the body; but bones are particularly picked out. The incidence of osteosarcoma in a study reporting in 1991 showed an unbelievable 50% increase. A report in 1955 in the New England Journal of Medicine showed a 400% increase in cancer of the thyroid in San Francisco during the period their water was fluoridated.

MY PARTICULAR CONCERN IS THE EFFECT OF
FLUORIDES 
ON THE THYRIOD GLAND

Perhaps I may remind you about thyroid disease. The thyroid gland produces hormones which control our metabolism – the rate at which we burn our fuel. Deficiency is relatively common, much more than is generally accepted by many medical authorities: a figure of 1:4 or 1:3 by mid life is more likely. The illness is insidious in its onset and progression. People become tired, cold, overweight, depressed, constipated; they suffer arthritis, hair loss, infertility, atherosclerosis and chronic illness. Sadly, it is poorly diagnosed and poorly managed by very many doctors in this country.

What concerns me so deeply is that in concentrations as low as 1ppm, fluorides damage the thyroid system on 4 levels.

1.  The enzyme manufacture of thyroid hormones within the thyroid gland itself. The process by which iodine is attached to the amino acid tyrosine and converted to the two significant thyroid hormones, thyroxine (T4) and liothyronine (T3), is slowed.

2.  The stimulation of certain G proteins from the toxic effect of fluoride (whose function is to govern uptake of substances into each of the cells of the body), has the effect of switching off the uptake into the cell of the active thyroid hormone.

3.  The thyroid control mechanism is compromised. The thyroid stimulating hormone output from the pituitary gland is inhibited by fluoride, thus reducing thyroid output of thyroid hormones.

4.  Fluoride competes for the receptor sites on the thyroid gland which respond to the thyroid stimulating hormone; so that less of this hormone reaches the thyroid gland and so less thyroid hormone is manufactured.

These damaging effects, all of which occur with small concentrations of fluoride, have obvious and easily identifiable effects on thyroid status. The running down of thyroid hormone means a slow slide into hypothyroidism. Already the incidence of hypothyroidism is increasing as a result of other environmental toxins and pollutions together with wide spread nutritional deficiencies.

14 MILLION EUROPEANS ARE AT RISK

One further factor should give us deep anxiety. Professor Hume of Dundee, in his paper given earlier this year to the Novartis Foundation, pointed out that iodine deficiency is growing worldwide. There are 141 million Europeans are at risk; only 5 European countries are iodine sufficient. UK now falls into the marginal and focal category. Professor Hume recently produced figures to show that 40% of pregnant women in the Tayside region of Scotland were deficient by at least half of the iodine required for a normal pregnancy. A relatively high level of missing, decayed, filled teeth was noted in this non-fluoridated area, suggesting that the iodine deficiency was causing early hypothyroidism which interferes with the health of teeth. Dare one speculate on the result of now fluoridating the water?

FLUORIDE DISPLACES IODINE IN THE BODY

These figures would be worrying enough, since they mean that iodine deficiency, which results in hypothyroidism (thyroid hormone cannot be manufactured without iodine) is likely to affect huge numbers of people. What makes it infinitely worse, is that fluorine, being a halogen (chemically related to iodine), but very much more active, displaces iodine. So that the uptake of iodine is compromised by the ejection, as it were, of the iodine by fluorine. To condemn the entire population, already having marginal levels of iodine, to inevitable progressive failure of their thyroid system by fluoridating the water, borders on criminal lunacy.

I would like to place a scenario in front of those colleagues who favour fluoridation. A new pill is marketed. Some trials not all together satisfactory, nevertheless, show a striking improvement in dental caries. Unfortunately, it has been found to be thyrotoxic, mutagenic, immunosuppressive, cause arthritis and infertility in comparatively small doses over a relatively short period of time.

DO YOU THINK IT SHOULD BE MARKETED?

Fluoridation of the nation’s water supply will do little for our dental health; but will have catastrophic effects on our general health. We cannot, must not, dare not, subject our nation to this appalling risk.

Dr Barry Durrant-Peatfield obtained his Medical degrees in 1960 at Guy’s Hospital London. He left the NHS in 1980 to specialise in thyroid illnesses drawing inspiration from the work of infamous Dr Broda Barnes, at the Foundation that bears his name, Connecticut, USA. He has been a medical practitioner for over forty years specialising in metabolic disorders during which time he became a leading authority in the UK for thyroid and adrenal management. For over twenty years he also ran a successful private clinic and became a nation-wide leading authority on thyroid and adrenal dysfunction, but clashed with establishment medicine in the management of thyroid illness. He is the author of The Great Thyroid Scandal (see opposite page), he currently lectures at nutritional colleges in London as well as conducting his own teaching seminars. Barry will shortly be opening a diagnostic clinic in the UK for thyroid and adrenal disorders where he will provide advice on diagnosis and treatment with special interests in nutritional aspects. For further information contact: Dr B Durrant- Peatfield 36A High St, Mersham, Redhill Surrey, RH1 3EA.

Tel: 44 (0)1737 215462 <mailto:Email: info@drpeatfield.com

Web site: http://www.drpeatfield.com

References:

L Goldemberg – La Semana Med 28:628 (1921) – cited in Wilson RH, DeEds F -”The Synergistic Action Of Thyroid On Fluoride Toxicity” Endocrinology 26:851 (1940).

G Litzka – “Die experimentellen Grundlagen der Behandlung des Morbus Basedow und der Hyperthyreose mittels Fluortyrosin”

Med Wochenschr 63:1037-1040 (1937) (discusses the basis of the use of fluorides in anti-thyroid medication, documents activity on liver, inhibition of glycolysis, etc.).

W May – “Behandlung der Hypothyreosen einschlieblich des schweren genuinen Morbus Basedow mit Fluor” Klin Wochenschr 16: 562 – 564 (1937).

Sarin: (GB: isopropyl methylphosono-fluoridate) is a colorless, odorless volatile liquid, soluble in water, first synthesized at IG Farben in 1938. It kills mainly through inhalation.

Cyclosarin (GF) and Thiosarin are variants. Pennsylvania Department of Health

http://www.dsf.health.state.pa.us/health/cwp/view.asp?a=171&q=233740

Sarin: (GB: CH3-P(=O)(-F)(-OCH(CH3)2)

Source: A FOA Briefing Book on Chemical Weapons http://www.opcw.org/resp/html/nerve.html Gerhard Schrader, a chemist at IG Farben, was given the task of developing a pesticide. Two years later a phosphorus compound with extremely high toxicity was produced for the first time.

IG Farben: “…the board of American IG Farben had three directors from the Federal Reserve Bank of New York, the most influential of the various Federal Reserve Banks. American IG Farben. also had interlocks with Standard Oil of New Jersey, Ford Motor Company, Bank of Manhattan (later to become the Chase Manhattan Bank), and AEG. (German General Electric) Source: Moody’s Manual of Investments; 1930, page 2149.”

http://reformed-theology.org/html/books/wall_street/chapter_02.htm

At a later date, Namaste will be publishing a more in-depth article outlining the devastating affects that fluoride, aspartame and MSG have on the endocrine system.

Dr Durrant-Peatfield will be answering frequently asked questions on thyroid illness in Namaste’s next issue. Send your questions to us preferably by

email to: info@namastepublishing.co.uk

.oOo.

Has anyone read the book, The Great Thyroid Scandal
by
Dr. Barry Durrant-Peatfield?

Does anyone know about the doctor? I saw that he has
had his license revoked for about 18 months due to
what his colleagues call bad medicine-
Seems like a mark in his favour.

EVIDENCE SHOWS FLUORIDATION A DANGER

by

Paul Connett, PhD Professor Emeritus of Environmental Chemistry,
St. Lawrence University, Canton, Director of Fluoride Action Network.

(See original article)

Currently, I am traveling in Italy giving presentations on waste management. I have been forwarded a copy of your editorial ridiculing any notion that fluoridation could possibly cause any health problem and that practice is extremely effective at reducing tooth decay.

I will leave your councilors to judge the quality of the evidence that I will share with them on March 14. I write now because I am upset with the bullying tone you have adopted with one of your councilors, Amy Valentine. It is well known that if people are unable to answer a disturbing message they begin by attacking the messenger. You have chosen to do so in this case using the authority of local dentists, the American Dental Association and the Centers for Disease Control and Prevention. However, on this particular issue all these sources are highly suspect because of their very aggressive and long-term promotion of this practice.

It is simply not enough to parrot the phrase that fluoridation is “safe and effective” to win the case. It is incumbent on those who support this most unusual practice (what other chemical is added to the public water supply to treat people rather than treat the water?), which has been rejected by most industrial countries, to provide the scientific evidence for their claims.

To offset the 23 studies from India, Iran, Mexico and China which have shown that high doses of fluoride are associated with lowered IQ in children, where are the studies of the IQ of children living in Plattsburgh or any other fluoridated community in the U.S.? I am not aware of any. Why have they not been done?

The key question, of course, is whether there is an adequate margin of safety between the levels which have caused this harm in other countries and the levels experienced by children in this country drinking uncontrolled amounts of fluoridated water. The lowest level estimated at which IQ was lowered in one of these studies was 1.8 ppm (Xiang et al., 2003). Can you find a single toxicologist or pharmacologist who will tell you that offers an adequate margin of safety for all children exposed to fluoridated water at 1 ppm? For that matter, will they also tell you that there is an adequate margin of safety for all the other health effects discussed in the 507-page report by the National Research Council, “Fluoride in Drinking Water” published in March 2006? Three of the authors of that report don’t think so and have stated so in public.

On the issue of effectiveness, where is the peer-reviewed, published, scientific evidence that the teeth of children in Plattsburgh are “sturdier” than children in non-fluoridated communities in the area? You have none — only anecdotal reports. In fact, a study commissioned by the N.Y. Department of Health, which examined tooth decay in third graders, found absolutely no relationship between tooth decay averaged by county and percentage of the county’s population drinking fluoridated water! Meanwhile, the data collected by the World Health Organization shows no difference in tooth decay in 12 year-olds between fluoridated and non-fluoridated countries .

In my view adding fluoride — a known toxic substance — to the public drinking water at 250 times the level naturally present in mother’s milk (0.004 ppm) is both reckless and foolish, especially now that even promoters of fluoridation like the CDC admit that fluoride works topically, not systemically, i.e. it works by acting on the surface of the tooth not from inside the body (CDC, 1999, 2001).

Not only did your editorial writer question my concerns about fluoride’s ability to damage the brain, but he or she also questioned my suggestion that fluoride also damages the teeth. That’s strange because the CDC has reported that 32 percent of American children have dental fluorosis, a mottling and discoloration of the teeth caused by ingesting fluoride before the permanent teeth have erupted.

While the largest proportion of children thus affected have the condition in its very mild form, over 3-4 percent of children have the condition in its moderate or severe forms, in which 100 percent of the enamel is affected. Moreover, while these enamel defects can be covered by expensive veneers (about $1,000 per tooth) the worrying aspect about this is that it is generally agreed that dental fluorosis is the first indication that the child’s developing body has been over-exposed to fluoride.

Thus, the key question then becomes, while the fluoride is damaging the growing tooth by some systemic mechanism, what other tissues might it be damaging without this obvious and visible telltale sign? This underlines the significance of the IQ studies from countries which do not have a fluoridation program to protect.

So let’s examine the science here, please, not just the reiteration of long-held beliefs.

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LETTER FROM –
PHYLLIS J. MULLENIX Ph.D
The Report That:
Brain Function Is Vulnerable To Fluoride…

Phylis M

Phyllis J. Mullenix, Ph.D.
P.O. Box 753 Andover, Massachusetts 01810-3347
5 May  1999

BSA Environmental Services
21403 Chagrin Boulevard
Suite 101
Beachwood, OH 44122
Re: Request for information on drinking water fluoridation

Dear Drs. Romoser-Breno and Beaver:

The April 15 request for comments regarding water fluoridation is vague in that no assurances are offered as to how my written opinion will be used. Thus, a copy of this letter will be sent to Mr. Gilbert Gonzales at Fort Detrick. Without the benefit of having read the “Environmental Assessment” report to which you referred to in your letter, I run the risk of being redundant with regard to the material already prepared. With these caveats, I offer the following comments about the advantages and disadvantages of water fluoridation.

To start, I must correct a statement you made in your letter regarding my being an “expert on drinking water fluoridation issues.” Prior to 1982, my knowledge of fluoride was limited to television commercials saying it was good for my teeth. Rather, my expertise was detection of neurotoxicity, which brought me to the Department of Psychiatry at Boston’s Children’s Hospital and Neuropathology at the Harvard Medical School. It was there that I met Dr. Jack Hein, Director of the Forsyth Dental Center and the scientist responsible for putting mono fluorophosphate (MFP) into toothpaste. Dr. Hein was a student of Dr. Harold Hodge, the chief pharmacologist on the Manhattan Project who conducted the world renowned studies on fluoride (1) and started water fluoridation. Dr. Hein invited me to Forsyth to study the neurotoxic potential of materials that dentists use, starting with fluoride, and we set up the first toxicology department in any dental research institution in the world. I was made Head of the department, and Dr. Hodge moved to Boston and became a member of my department where he stayed until his death in 1990. Another Manhattan Project scientist and fluoride researcher, Dr. Ben Amdur, also joined the department.

My investigations of the neurotoxicity of fluoride started in 1987. Using a new computer pattern recognition system capable of a sensitivity and objectivity other behavioral measures did not possess, we studied an animal model first developed for the study of dental fluorosis. Frankly, we expected to find nothing. The results from the first experiment we thought must be wrong, so we kept repeating the study with more animals, different doses, sexes, ages and methods of administration. Like quicksand, every effort we made sank us further into the realization that brain function was impacted by fluoride. Scientific integrity dictated that we publish our results (2,3), but employed at a dental research institution made us weak in the knees to do so.

In our 1995 paper (2), we reported that brain function was vulnerable to fluoride, that the effects on behavior depended on the age at exposure and that fluoride accumulated in brain tissues. Rats exposed as adults displayed behavior-specific changes typical of cognitive deficits, whereas rats exposed prenatally had dispersed behaviors typical of hyperactivity. Brain histology was not examined, but the behavioral changes were consistent with those seen when hippocampal development is interrupted and memory problems emerge. Overall, we concluded that the rat study flagged potential for motor dysfunction, IQ deficits and/or learning disabilities in humans.

Criticisms of our study by dentists say that our results in rats are not relevant to humans because the doses we used were too high (75-125 pprn NaF in drinking water). These criticisms are without merit because our doses in rats produce a level of fluoride in the plasma equivalent to that found in humans drinking 5- 10 ppm fluoride in water, or humans receiving some treatments for osteoporosis. This plasma level is exceeded ten times over one hour after children receive topical applications of some dental fluoride gels. Thus, humans are being exposed to levels of fluoride that we know alters behavior in rats. Perhaps dentists see no problem with this fact, but scientists involved with toxicity risk assessment will view it differently. The fluoride levels in the drinking water of our rats were not high, they were taken from the well known animal model developed for the study of dental fluorosis, a model used repeatedly by dental researchers for several years.

Other criticisms of equal absurdity have been expressed by dentists about our study. However, they are not important to dwell upon now because that first study was but one piece of an emerging picture. Soon after our study was published, we learned of two epidemiology studies from China showing IQ deficits in children over-exposed to fluoride via drinking water or soot from burning coal (4,5). Next, we found a literature review that assembled case reports spanning 60 years on neurological effects in humans exposed to fluoride (6). A common theme in these reports was that fluoride exposure impaired memory and concentration and that it caused lethargy, headache, depression and confusion. The depression is not something to ignore because suicide occurs more frequently than expected in populations of fluoride workers (7).

More recently, another laboratory investigation found that chronic exposure to fluoride (I ppm) in drinking water of rats compromised neuronal and cerebrovasculature integrity (blood brain barrier) and increased aluminum concentrations in brain tissues (8). Another study found that fluoride in drinking water of rats decreased membrane lipids important to proper brain function (9). Moreover, the latest studies have shown that fluoride accumulates in human and animal pineal glands where it impairs melatonin production (10, 11), a finding critical when it is considered that melatonin is an agent that protects the central nervous system from radiation by scavenging free radicals (12). Finally, there is a recent study published which reports that silicofluorides in fluoridated drinking water increase levels of lead in children’s blood, a risk factor that predicts higher crime rates, attention deficit disorder and learning disabilities (13).

Unfortunately, the link between fluoride and the brain does not end with the above mentioned studies. In 1993 while studying the neurotoxicity associated with the treatments of childhood leukemia, we demonstrated that the fluorinated steroid dexamethasone disrupted behavior in rats to a greater degree than did its non-fluorinated counterpart prednisolone  (14,15). This finding prompted a clinical study of children treated for leukemia, where it was found that the fluorinated steroid was more detrimental to IQ than the non-fluorinated steroid, in particular reading comprehension, arithmetic calculation and short-term working memory deficits were greater (16). In short, this finding has fueled a growing concern about the contribution of fluorinated pharmaceuticals to the total body burden of fluoride.

As you decide whether or not to fluoridate the water supplies of Fort Detrick, it is imperative that you consider the impact on total body burden of fluoride. The soldier today is a different individual, facing a very different situation than that encountered fifty years ago when fluoridation was promoted as a “safe and effective” means to protect against tooth decay. The difference stems from the fact that 1) fluoride exposures today are out of control, well beyond the dose touted as optimum for caries prevention; and 2) people today, especially soldiers, are exposed to substances and conditions that will interact with fluoride exposure and magnify harmful effects (i.e., exposure to beryllium, lead, strontium, aluminum, cholinesterase-inhibiting pesticides, uranium hexafluoride, stress, nutritional deficiencies, increased water consumption due to extreme exercises, fluorinated pharmaceuticals, and nerve gases including sarin).

In summary, my opinion is that there are no advantages to water fluoridation. The risks today far exceed the hoped for benefit. Dr. Hodge during the Manhattan Project requested funds from Col. Stafford L. Warren to do animal experimentation to determine central nervous system effects of fluoride (17). He did so because he had clinical evidence that the fluoride component of uranium hexafluoride caused “mental confusion, drowsiness and lassitude among the workmen. Yet, he never got to do those studies, and because this information was classified, he never discussed his findings with me. Perhaps, however, this explains why he was so intensely interested in my fluoride studies up to the time of his death.

Therefore, in good conscience I can only discourage the notion of fluoridating the water supply of Fort Detrick. The evidence against the safety of this public health policy will keep mounting and never disappear again. My ignorance of fluoride in the beginning was a matter of chance. If you ignore this evidence today, it will be a matter of choice.

Good luck with doing the right thing.
Sincerely,
Phyllis J. Mullenix, Ph.D.

F. Hormone disruptor ss

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Chronic Fatigue Syndrome

FLUORIDE:
DAMNING NEW EVIDENCE

Extract  from:

“What Doctors Don’t Tell You” 
March 1999
Researcher Doris Jones has unearthed startling
new evidence demonstrating that fluoride
interferes with enzymes systems, damaging
many organs systems of the body.

Extract:

…. While much has been written about the effects of too much fluoride on teeth and bones, little is known about the effects of fluoride on the rest of the body. But new evidence has emerged demonstrating that it has devastating effects on just about every organ in the body, and may even be partly responsible for behavioral problems like hyperactivity and many puzzling illnesses like ME. (Myalgic Encephalomyelitis /Chronic Fatigue Syndrome), The late fluoride critic George L Waldbott discovered that, besides teeth and bones, fluoride can damage soft tissue. According to his research, the small fluorine ion with a high-charge density can combine with other ions and penetrate every cell in the body. It interferes with the metabolism of calcium and phosphorus and the function of the parathyroid glands. It has a strong affinity to calcium, but will also readily combine with magnesium and manganese ions and so can interfere with many enzyme systems that require these minerals. The interruption of these enzyme systems, in turn, may disturb carbohydrate metabolism, bone formation and nerve-muscle physiology. Indeed, every vital function in the body depends on enzymes; because fluoride easily reaches every organ, many diverse toxic symptoms can result.

“Most diseases are results of disturbances of the enzyme systems,” says Professor Abderhalden. “Damage due to fluoride could be shown on 24 enzymes.” Enzyme systems react to fluoride in different ways; some are activated, others are inhibited. Lipase (essential for the digestion of fat) and phosphatases are very sensitive to fluoride. In patients with skeletal fluorosis, succinate dehydrogenase activity is inhibited. In chronic fluoride poisoning, this diminished enzyme activity accounts for muscular weakness and even muscle wasting. Human salivary acid phosphatase is diminished by half when exposed to 3.8 ppm of fluoride, while blood enzyme cholinesterase is inhibited by 61 per cent on exposure to 0.95 ppm fluoride-a level within recommended levels. So what does this do in the body? (Author, Handbook of Experimental Pharmacology, Springer Verlag, 1970: 48-97).

Alkaline phosphatase, an enzyme involved in bone growth and liver function, may also be poorly affected by low-level fluoride intake. According to scientists from the Department of Chemistry of the University of California at San Diego, fluoride switches off an enzyme by attacking its weakest links-the delicately balanced network of hydrogen bonds surrounding the enzyme’s active sites (J Biol Chem, 1984; 259: 12984-88).

Their particular studies concerned the enzyme cytochrome C oxidase, an oxygen-carrying respiratory enzyme; deficiencies of this vital enzyme have been linked to cancer, severe diseases and even cot death.

It’s also been shown by research at Kings College in London that fluoride forms very strong hydrogen bonds with amides, which are formed when amino acids join together to form a protein (J Am Chem Soc, 1981; 103: 24-8). This can also cause chromosomal damage. If the protein is greatly distorted, the body’s immune system no longer recognizes it, treats it as a foreign protein and will try to destroy it, which in turn triggers allergic skin or gastrointestinal reactions (J Yiamouyiannis, Fluoride: The Aging Factor,. Delaware, Ohio: Health Action Press, 1993: 94-9). 

Stomach and bowel disorders are the main features of fluoride intolerance. Even small amounts of fluoride can form hydrofluoric acid in the stomach to produce gastric pains, nausea and vomiting. Young children are particularly at risk. Fluoride tablets can even cause gastric hemorrhages; in one instance, a 9-year-old boy sustained such damage that he required the removal of large parts of his stomach (Fluoride, 1977; 10: 149-51).

The most readily identifiable feature of soft-tissue fluorosis is extraordinary general fatigue, which is frequently linked to thyroid deficiency. The thyroid gland requires iodine to produce the hormone thyroxine, which controls the rate of metabolism in the body. But when fluorine is present, it displaces iodine, which will cause a thyroid gland to stop working properly (K Roholm: Fluor and Fluorverbindungen, in: Handbuch Experimenteller Pharmakologie, Ergaenzungswerk, Vol.7, Springer, 1938: 20).

The parathyroid gland, which regulates the distribution of calcium and phosphorus in the body, is extremely sensitive to excessive amounts of fluoride. Over fifty years ago, Indian clinicians found a close relationship between skeletal fluorosis and hyperparathyroidism (J Hyg 1942; 42: 500-4).

Fluoride has even been shown to affect the pituitary gland, which controls growth rate by regulating the production of thyroid hormones (Seances Soc Biol Fil, 1930; 103: 981-2). In animals, less than normal amounts of thyroid hormones are produced when animals are given water containing a fluoride content equivalent to that of artificial water fluoridation (Bull Schweiz Akad Med Wiss, 1954; 10: 211-20). Using scanning electron-microscope photographs, Professor AK Susheela of the Fluoride and Fluorosis Research Foundation of India and Senior Consultant to the Indian government, who has published over 100 scientific papers on the hazards of fluoride, proved that when exposed to fluoride, red blood cells are killed prematurely, lowering haemoglobin and causing anaemia.

She also showed that calcium levels diminish as fluoride levels in the body rise; the gastrointestinal tract mucosa is damaged, causing irritable bowel syndrome; and blood fluoride levels rise continuously with prolonged use of fluoridated toothpaste.

When people are bombarded with fluoride, in the form of fluoridated water, toothpaste and mouth rinses, muscles and elements of connective tissue, particularly collagen fiber and bone tissue, undergo degenerative changes.

At the 1998 US Conference of the International Society for Fluoride Research in Bellingham, Washington, Dr Jennifer Luke from the University of Surrey, UK, presented evidence on the effects of low and high doses of fluoride on the pineal gland in gerbils. In both gerbils and humans this gland helps control the aging process and the production of melatonin, which regulates the sleep/wake cycle. Gerbils exposed to a high level of fluoride experienced a significant decrease in the production of melatonin, and earlier genital maturation. While animal studies may not always be applicable to humans, Dr Luke theorized that mass fluoridation may be behind the general decline in the age of puberty in the West (Fluoride, 1998; 31: 4: 175).

In areas where water is fluoridated, evidence shows that dangerously high fluoride concentrations accumulate in many soft tissues and organs of the population, including the heart, kidney and bladder; the highest level ever recorded-8400 ppm-was found in the aortas of people living in Grand Rapids, Michigan, where fluoride was first introduced in America.

The heart and blood vessels are affected by fluoride. Cardiac irregularities and low blood pressure have been noted in experimental poisoning using large doses (Publ Health Report, 1956;71:459-67). In 1950, five years after experimental introduction of fluoride into drinking water in Grand Rapids, Michigan, the number of deaths from heart disease nearly doubled (The Grand Rapid Herald, July 28, 1955). Death rates due to cancer, intracranial lesions, diabetes and arteriosclerosis were all markedly increased compared to death rates per 100,000 in the entire state.

In electrographic studies, Japanese researcher Taka Mori showed a direct link between damage to the heart and dental fluorosis in children who drank water with a fluoride content of 0.5-6.2 ppm. Fluoride also affects arteries, causing bruise-like skin lesions called “Chizzola maculae’”, showing inflammatory areas around capillary blood vessels. Because fluoride attracts calcium, it contributes to their hardening. Fluoride affects the brain and entire central nervous system. Neurological problems like headaches, vertigo, spasticity in extremities, visual disturbances and impaired mental acuity can all result. Tissue damage to anterior horn cells has been found (Fluoride,1975;8:61-85). Official annual statistics revealed that death rates among malnourished children in the Chilean town of Curico, fluoridated since 1953, were to 104 per cent higher than in comparable, non-fluoridated towns, and the general mortality was higher by 113 per cent, compared with the average for the country (Ziegelbecker R et al, Journal? 1995:47-48).

Fluoride, hyperactivity and violence.
- Several studies have shown that exposure to fluoride can cause behavioral changes (Int Clin Psychopharmacol, 1994;9:79-82; Neurotoxicol and Teratol, 1995;17:169-77; Fluoride, 1996;29:187-88) At a 1998 Conference on Fluoride, Professor Roger Masters reported a link between the blood lead levels of 280,000 children in Massachusetts and the use of silicofluorides for water fluoridation. Here and in Georgia, behaviors associated with lead toxicity, such as violent crime, are more frequent in communities using silicofluorides than in areas not using them. At the same conference Dr Phyllis Mullenix reported results of a study using two steroids to treat childhood leukemia, one of which had a fluorine atom in its structure. In the study, this steroid caused behavior patterns typical of hyperactivity. A follow-up study of children using this drug for two years showed a significant drop in average IQ scores, compared with children using the non-fluoride drug (Fluoride, Nov.1998;31;4:175).
In one family in Glasgow, every member is severely affected by fluoride-the mother experienced an anaphylactic shock to Prozac, which contains fluorine, and all four children exhibited erratic/violent behavior and suffered from immune system damage on exposure to fluoride (in their drinking water?

Fluoride And ME
 A[l]though few researchers have looked at the role of fluoride in the development of ME, there are conspicuous similarities between key features of ME/CFS and those seen in the very early stages of chronic fluoride intoxication (Fluoride,1998; 31:13-20)

Dr John McLaren Howard of Biolab in London offers a few important clues why. He discovered that ME patients experience reduced movement of white blood cells when exposed to quite low levels of fluoride (Inter Action 14, Autumn, 1994:53-54). This effect on white blood cells might render patients less able to fight infections efficiently, or lead to an exacerbation of their health problems.

Fluoride also interferes with phagocytosis, as well as causing the release of superoxide free radicals in resting white blood cells. This means that fluoride slows down and weakens the very cells which serve as the body’s defense system; bacteria, viruses, chemicals and the body’s own damaged or cancerous cells are then allowed to wreak havoc. Minor infections take longer to throw off and cause more serious illness (John Yiamouyiannis, The Aging Factor, Health Action Press, 1993:p32). This is precisely what appears to be happening in many cases of ME.

We do not know how many children or teenagers had topical high concentration fluoride dental treatment before succumbing to infections which led to ME/CFS. My son had fluoride treatment to prevent tooth decay in the autumn of 1979, after which his health dramatically deteriorated, commencing with gastric problems, various minor infections, then glandular fever, followed by atypical measles, more infections and eventually resulting in ME in 1980. In the end the fluoride treatment didn’t work in preventing tooth decay-he’s needed 15 fillings over the past nine years.

The American pathologist Majid Ali explains that chronic fatigue results due to “accelerated oxidative molecular injury”. Only a well functioning enzyme system can protect us from such injury and maintain normal energy levels. In chronic fatigue there is a high frequency of membrane deformities, due to increased oxidative stress on the cell membranes, which is why sufferers lack energy. Interestingly, Ali also highlights gastrointestinal disturbances, such as IBS, as playing a significant part in chronic fatigue (The Canary and Chronic Fatigue, Life Span Press, 1994).

Many ME patients have an under active thyroid (InterAction 27, Sept.1998:27). Chronic fatigue and exhaustion due to hypothyroidism is a cardinal feature in the Chronic Fluoride Toxicity Syndrome.

Experienced researchers who have studied ME for decades maintain that as with polio, it is damage to anterior horn colles caused by a gut virus, which explains why polio victims are paralyzed or suffer from impaired motor function (The Clin and Scientific Basis of ME/CFS). But fluoride has also been shown to damage anterior horn cells. Gastrointestinal disturbances, often referred to as IBS, are also known to play a significant part in ME, as they are in the Chronic Fluoride Toxicity Syndrome.

Severe sleep disturbances, or reversal of sleep rhythm, are a common feature in ME/CFS (Clin). Deposits of large quantities of fluoride in the pineal gland of animals have caused similar problems (J Luke, Bellingham Conference, 1998).

At this point, no one knows to what extend these syndromes overlap, or fluoride or fluorine facilitates the development of ME by various biological agents. The indications are that fluoride may act as a “facilitating co-factor” and exacerbate existing problems in such patients. Or it could be, as Dr H C Moolenburgh suggests, that ME is one of the end stages of a general chemical poisoning, with fluoride one of the worse offenders (personal communication, 7.1.1999). Although many unanswered questions remain, one thing can be said with certainty. Fluoride not only is not beneficial, but may turn out to be one of the major factors in the serious health problems besetting modern man.

Doris Jones 
© What Doctors Don’t Tell You Ltd. 1998

  Pub med  

FLUORIDES – Toxic profile  – U.S. Dept. of Health Services

CANADIAN ENVIRONMENTAL PROTECTION ACT-

Inorganic Fluorides-A review-R.G.Foulkes

The web site below is not a fluoride issue but it does illustrate
that the FDA does NOT care about the American People
only the profits of the drug companies.
Dr. Burzynski’s work threatens the viability of the cancer industry

See: www.BurzynskiMovie.com

Winner H V Award ss

Comment by 'Variety' ss

www.BurzynskiMovie.com

Go to: ↓

RESEARCH PAPERS – A —

fluoridation-queensland-logo

 

new-devider-fq

7704d57a00f4d8802b5296134c4eb5c8

F. Never!

 

On the same topic:

THE PINEAL GLAND

A Short Selection Of Comments

From Famous Researchers

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rodger-d-master-f

With special thanks to Rodger D. Masters.

THE SOCIAL IMPLICATIONS OF NEUROSCIENCE:

LINKING BRAIN BIOCHEMISTRY AND VIOLENT CRIME

Roger D. Masters (Dartmouth College)·

THIS FILE IS A DRAFT OF THE CHAPTER WITH THIS TITLE IN:

Richard W. Bloom and Nancy Dess, eds.,

Evolutionary Psychology and Violence:

A Primer for Policymakers and Public Policy Advocates

(Westport: Praeger, 2003), pp. 23-56.

ABSTRACT

It is impossible to deny that a revolution in neuroscience and other areas of biology has taken place over the last half-century.  The  estimates of 83 million Americans taking drugs like Prozac for depression and 11 million children on Ritalin for hyperactivity indicate it is time to reconsider the role of brain chemistry in social behavior and violent behavior.  Since it is obvious that loss of impulse control can contribute to violent outbursts – and evidence shows that some toxic chemicals (such as lead) can have this effect, it is time to consider neuroscientific evidence linking environmental toxins and rates of violent behavior.  To illustrate the implications of the new issues involved, I focus on a hitherto unexplored example.  Two chemicals (H2SiF6 and Na2SiF6, jointly called “silicofluorides” or SiFs) are used to treat public water supplies of 140 million Americans even though, as the EPA has admitted, they never been tested for safety.  To illustrate the interdisciplinary complexities entailed when linking brain chemistry to policy decisions concerning violent crime, our argument has four main stages: first, why might SiFs be dangerous? Second, what biochemical effects of SiF could have toxic consequences for humans?  Third, on this basis a research hypothesis is formulated to measure the types of harm.  In this case, we predict children in communities using SiF should have increased uptake of lead from environmental sources and higher rates of behavioral dysfunctions such as hyperactivity (ADHD) known to be caused by lead neurotoxicity.  Finally, the hypothesis is tested using multiple sources of data including rates of violent crime studied using a variety of multivariate statistical techniques (including analysis of variance, multiple regression, and stepwise regression).  As this outline should make clear, a combination of interdisciplinary perspectives and great prudence is needed to link research in neuroscience to policies concerning violent crime,  If confirmed, however, the potential benefits of hypotheses like the one tested below may be great, revealing the generally unsuspected value of including neuroscientific research in the analysis of human social behavior.

Requests for reprints and correspondence should be directed to: Prof. Roger D. Masters, Department of Government, HB 6222, Dartmouth College, Hanover, NH 03755. Email:  Roger.D.Masters@Dartmouth.edu

The full version of the above is on the net,

and as the above suggests adding silicofluorides

to drinking water amounts to domestic terrorism.

 Editor’s note:

Zinc deficiency can account for bad behaviour – F. is an antagonist of zinc.

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Fluoride and Crime in the USA

Original  →  HERE

SUMMARY:

A four-part study explores possible connections between 

water fluoridation and crime in America.

Part A, Media-reported crime database and fluoridation, presents an observational database of violent crimes, mostly multiple shootings, and finds an unusually high percentage of them associated with water fluoridation, suggesting the existence of a “fluoride-related” category of crime. A low-end threshold for the toxic effects of fluoridation of 0.3 ppm is identified, and the term “fluoridated” is defined here as having a fluoride level of 0.3 ppm or higher. In Part B, Online crime database and fluoridation, a published database of year 2000 crime data for 327 US cities over 75,000 population, representing 80 million Americans, was expanded to include fluoridation data for these cities. Water fluoridation was consistently associated with high crime rates at all population levels. Part C, Book crime database and fluoridation, examines year 2000 crime statistics for six major crimes in the same 327 cities according to their fluoridation status. Cities having natural fluoridation, or which use silicofluorides or sodium fluoride, are shown to have substantially higher crime levels than nonfluoridated cities. Part D, Lead related crime, quantifies the amount of crime historically associated with lead intoxication, thus identifying a remainder which may be associated with fluorides. This study presents a data-backed hypothesis about one possible cause of crime; it is not a definitive statement about crime causality.

Keywords: Crime; Fluoridation; Fluoride toxicity; Lead toxicity; School shootings; USA.

INTRODUCTION

In 1999 I observed that nine of ten randomly-selected school shootings in America had occurred in fluoridated communities, and that the shooter in the tenth had used Prozac, a fluorinated pharmaceutical.b With less than 60% of the U.S. population fluoridated, a non-random correlation between fluoride and violence was suspected.

Others have connected fluorides with violence. Grandjean et al identified significantly elevated mortality due to violence and suicide among Danish cryolite workers.1 Several studies have examined effects of fluoride on mental development, brain function, and behavior. Li et al, Zhao et al, and Xiang et al showed that high fluoride exposure reduces intelligence in children.2-4 Varner et al documented the effects of aluminum fluoride and sodium fluoride with neuronal damage, dementia, and mortality in rats.5,6 Mullenix et al documented detrimental CNS effects of sodium fluoride in rats, showed that timing of fluoride (a).

Correspondence: Jay Seavey, AIA emeritus, P.O. Box 5234, Manchester, NH, USA 03108-5234. E-mail: jayseavey1618@earthlink.net bKip Kinkle murdered his parents, then killed 2 and wounded 22 in a school shooting on 5/21/98 in unfluoridated Springfield, OR. The police report indicated that he had previously been treated with Prozac [fluoxetine hydrochloride]. A structural formula for Prozac appears in Physicians’ Desk Reference, 53rd ed., Montvale NJ: Medical Economics; 1999. p. 924. The other nine fluoridated locations noted at the time were: Moses Lake, WA; Bethel, AK; Pearl, MS; West Paducah, KY; Jonesboro, AR; Edinboro, PA; Fayetteville, TN; Littleton, CO; and Taber, Alberta, Canada. My observations were made at a public hearing on fluoridation held in Manchester, NH, and reported in The Union Leader (Manchester, NH)1999 Sept 23, Sect. A:1,20.

 Fluoride 2005;38(1)

12 Suavely [?] exposure can be developmentally critical, identified sex-linked differences in some of these effects, and demonstrated fluoride accumulation in the brain.7 Others have explored heavy metal intoxication with and without fluorides, and their mental and behavioral effects. Needleman et al showed psychological impairment and behavioral deficits in children from lead exposure.8 Masters and Coplan focused attention on elevated blood lead levels when silicofluorides are used for water fluoridation.9 Other work by Masters et al addressed manganese and lead toxicity, and silicofluoride use, relative to crime, alcoholism, and cocaine/crack abuse; and identified a time lag between the removal of lead from gasoline, and a later decline in crime rates.10 Fluoride, by itself and in conjunction with heavy metals, appears to alter brain function and to predispose some humans to violence. It seemed timely to study more directly the relationship between fluoridation and crime: cumulatively, these earlier studies led to an expectation that such a relationship could be demonstrated.

The work reported here is divided into four parts, A, B, C and D. They evolved sequentially over about four years, and do not reflect a methodology adopted from the outset.

MATERIALS AND METHODS

Part A: Media-reported crime database and fluoridation

Stories were accumulated from news mediaa over a period of approximately two years and assembled into a database (“A”) of 152 events, most of which occurred between 1993 and 2001 (media stories sometimes reported sequelae, such as court proceedings). The stories were primarily of multiple shootings, but also included unexecuted events involving weapons and similar ideation. The database also included some stabbings, drownings, arsons, and bombings, the

A The collecting of news stories utilized The Union Leader (Manchester, NH), and America Online; many of the stories from these sources originated from The Associated Press or from Reuters. The stories were selected, based on their content and on my intuition, from my routine daily reading, rather than from a methodical or exhaustive search using, for example, keywords or search engines. Events were typically multiple murders, usually with firearms, having an apparent “senseless” character to them. Events with known motives (except crimes grossly disproportionate to their motives), or which were known to be gang-or drug-related, were excluded. Domestic violence was excluded unless the victims included children. Stories were typically clipped, or were downloaded and printed, and placed in a file; periodically, the file would be reviewed, and the fluoridation status of the locations and of the perpetrators would be determined using the Fluoridation Census 1992. American Automobile Association roadmaps for the entire United States were regularly consulted to gain information about locations mentioned in news stories. In many cases telephone calls were made to get detailed information about local water systems. Calls were also made, with far less success, to get information about perpetrators and their life histories. Law enforcement personnel were generally reluctant to divulge much in the aftermath of an event, while it was still being investigated. Efforts to gain information from news writers were equally fruitless. In many instances, a succession of news stories over a period of time was needed to extract basic information about an event, as the initial reporting about a multiple shooting might be sketchy. On several occasions, after a major event, the news sources carried a list of 10 or 15 similar events—school shootings, workplace shootings, etc. These event lists, if they included events I had not already listed, were typically searched out using the Internet. This, along with current reporting of event sequelae [squealed], such as court proceedings, provided an avenue for including events going back several years. These lists also provided a basis for comparison: by the time I had accumulated 152 events, the database was more inclusive, by a factor of ten, than the longest of these lists which the media had presented; yet it is by no means deemed to be exhaustive.

Fluoride 2005;38 (1)

Water fluoridation and crime in America 13 common denominator being the heinous and senseless character of the crimes, and an absence of apparent motive. In each case, after an event was identified for inclusion in the database, a search was later made to determine the fluoridation status either of the place where the event occurred, or of the place where the perpetrator lived. A fluoridated community is defined for this study as one having a fluoride level of 0.3 ppm or more in the public water supply.a A statistical analysis was then performed, comparing the “fluoridation-connection” of the collected events with the nationwide fluoridation level. As a control, database “B” was developed, utilizing 164 randomly selected stories published between 1993-2001 in “The Armed Citizen”, a regular column in American Rifleman, a monthly magazine published by the National Rifle Association. These stories reported incidents in which firearms were used by citizens for self-defense.

Part B: Online crime database and fluoridation

Noting that Part A was somewhat limited by the particular type of crime it focused on, I broadened the search to include publicly-available data on a wider category of crimes. A database by Morgan Quitno Press (MQP), Lawrence, Kansas, published in book form and posted online, listed crime data for the year 2000 for 327 American cities having populations over 75,000, and rated their comparative safety according to a score or index which represented their aggregate incidence, based on FBI crime statistics, for six major crimes: murder, rape, robbery, aggravated assault, burglary, and motor vehicle theft.11,12 The score for each of the 327 cities was referenced to a national average of 0.00, and

aThe U.S. Public Health Service has generally defined “fluoridated” water as having a fluoride level at or above 0.6-0.7 ppm. The reason for selecting a lower level of 0.3 ppm to define “fluoridated” for the purposes of this study is as follows: Human physiology has some capacity for detoxifying and eliminating fluorides. Dental fluorosis offers the most readily-available and visible indicator for fluoride intoxication. Therefore, if we can establish a level below which this toxicity is not evident, it provides at least a speculative basis for considering that other toxic effects we are hypothesizing about may also not manifest themselves below this level. In other words, we are not interested in a level above which some hypothetical dental benefit allegedly occurs; we are concerned, rather, with the level below which toxic effects are not in evidence. H. Trendley Dean, DDS, in “Epidemiological studies in the United States” (In: FR Moulton, editor. Dental Caries and Fluorine. Washington, DC: American Association for the Advancement of Science, 1946. p. 5-31.) provides data from America necessary to make this determination. While Dean does not identify 0.3 ppm as a definitive cut-off level for the appearance of dental fluorosis, his tabulated data in Table XI, page 23, show that the prevalence of dental fluorosis begins to rise sharply above a fluoridation level of 0.3 ppm, and that the few observed cases occurring below this level are characterized as “very mild”. The appearance of dental fluorosis probably does not hinge solely on fluoride in drinking water; it probably reflects nutrition in general, and the mix of other minerals in the drinking water. Fluoride exposure relates partly to diet, being high, for example, in a diet high in seafood. The toxic manifestations of fluoride, it is believed, are also reduced by activities which remove fluoride from the system, such as hot-water bathing or sweat bathing. There is a discussion in Fluoridation: The Great Dilemma (Waldbott GL, Burgstahler AW, McKinney HL. Lawrence KS: Coronado Press, 1978. p. 180), of significant levels of dental fluorosis on the South Atlantic island of Tristan da Cunha, where the fluoride level is 0.2 ppm. This, however, seems to be the extreme end of the spectrum, and it may reflect a diet high in fish, but possibly relatively deficient in Vitamin C, calcium, and/or magnesium. For all of these reasons, but particularly on the basis of Dean’s American data, 0.3 ppm and above was chosen to define the term “fluoridated”. It is not suggested that fluoridation levels below 0.3 ppm have no toxicity, or that this represents a “safe” level of fluoride in water.

Fluoride 2005;38(1)

14 Seavey

scores ranged from –84.94 (safest) to 373.28 (most dangerous). The MQP database for its “Safest Cities Award” includes nearly 80 million Americans—about 28.5% of the U.S. population. a I modified this database by adding fluoridation data for each of the 327 cities, and then sorted the list into six groups by population size. Within each group, cities were listed according to increasing “score” or “crime index”. Each of the six groups was then bifurcated, to identify a Low Crime subgroup and a High Crime subgroup within each population group. Total fluoridation incidence for each of the six population groups was determined, and its percentage was calculated. These percentages determined the expected fluoridation incidences for the Low Crime and High Crime subgroups within each population group. Expected incidences were then compared with observed incidences for each of the 12 subgroups, and the differences were noted. (See Table 1.) A two-way table of the differences was developed, and the chi-squared statistic was calculated. (See Table 2.)

Part C: Book crime database and fluoridation

MQP does not tell us in City Crime Rankings, 8th edition, what formula was used to generate scores for its “Safest City Award.” While these scores are said to allow a direct comparison of cities on the basis of their crime rates, we are not told how these scores or crime index figures can be translated into actual crime rates, and thence, using population data, into actual numbers of crimes. For this reason, I have used MQP’s more detailed published crime rate data, to develop this information.13 For each of the 327 cities, actual year 2000 rates for each of the six major crimes were entered and then totaled into an aggregate crime rate for each city. Fluoridation data were then entered for each city. The 327 cities were then sorted in database “327” according to their fluoridation status. Within each of the fluoridation categories, the cities were sorted by ascending aggregate crime rate.

Part D: Lead related crime

The connection between lead intoxication and criminal behavior appears to be well established.9 The phase-out of leaded gasoline began in the U.S. in 1976;14 airborne pollution from this source was the primary cause of lead intoxication, with lead from paints and from solder in food cans generating further exposures.

As documented by the National Health and Nutrition Examination Surveys (NHANES) blood lead levels in Americans aged 1–74 declined by 78% between 1978 and 1991, and by 76% in ages 1–5. 15 Subsequent research shows the aIt is stated on p.1 of City Crime Rankings11 under the heading “Methodology”: “First, city and metro crime rates for six basic crime categories—murder, rape, robbery, aggravated assault, burglary and motor vehicle theft—were plugged into a formula that measured how a particular city or metro area compared to the national average for a given crime category. The outcome of this equation was then multiplied by a weight assigned to each of the six crime categories. For this year’s award (2000), each of the six crimes was given equal weight. By weighting each crime equally, cities are compared based purely on their crime rates and how they stack up to the national average for a particular crime category. These weighted numbers then were added together for a city or metro area’s final score.”

Fluoride 2005;38(1)

Table 1. 327 Cities grouped by population, with groups bifurcated into high and low crime sub-groups

Population Group Size

Crime level subgroup

[N/2 or (N-1)/2]

High [24]

Low [24]

High [18]

Low [18]

High [22]

Low [22]

High [15]

Low [15]

High [31]

Low [31]

Average crime index

[Difference between the high & low subgroups]

183.51

42.93 [140.58] [10.26%]

120.81 268,888

-0.57 252,535 [121.38] [6.48%]

120.73 176,726

7.09 178,424 [113.64] [0.96%]

92.29 134,370

-34.56 134,213 [126.85] [0.12%]

61.35 110,713

-42.89 110,342 [104.24] [0.34%]

Fraction of population group fluoridated

[%]

41/48 [85.417]

26/37 [70.270]

25/44 [56.818]

16/30 [53.333]

34/63 [53.968]

63/105 [60.000]

Fluoridation status of population subgroups based on the fraction of the population group fluoridated

>350,000 (C) [48]

200,000– 350,000

(D) [37]

150,000– 200,000

(E) [44]

125,000– 150,000

(F) [30]

100,000– 125,000

(G) [63]

75,000– 100,000

917,401

High 63.46 85,667 [52]

(H) [105] Low -44.62 85,453

[52]

[108.08] [0.25%]

Water fluoridation and crime in America 15

 (Data- base)

[N]

Average population size

[% difference in population

size]a

832,072

Number expected to be fluoridated

20.50 20.50

12.65 12.65

12.50 12.50

8.00 8.00

16.73 16.73

31.20 31.20

Number observed to be fluoridated

23.00 18.00

15.00 10.00

16.00 9.00

12.00 4.00

18.00 16.00

34.00 29.00

Difference between observed & expected

+2.50 -2.50

+2.35 -2.65

+3.50 -3.50

+4.00 -4.00

+1.27 -0.73

+2.80 -2.20

a The % difference in population size was calculated by taking the difference in the average population between the two subgroups, dividing by the size of the smallest group, and multiplying by 100.

Fluoride 2005;38(1)

16 Seavey

Table 2. Chi-squared statistics for 327 cities grouped by population, with groups bifurcated into sub-groups by crime level and fluoridation status

Population Group Size

Expected (based on the fraction of the population group non-fluoridated) and observed numbers of non-fluoridated population subgroups

Crime level subgroup

[N/2 or (N-1)/2]

High [24]

Low [24]

High [18]

Low [18]

High [22]

Low [22]

High [15]

Low [15]

High [31]

Low [31]

75,000– 100,000 [52]

(H) [105] Low [52]

Expected (based on the fraction of the population group fluoridated) and observed numbers of fluoridated population sub- groups

(Database)

[N]

Number expected to be

fluoridated

20.50 20.50

12.65 12.65

12.50 12.50

8.00 8.00

16.73 16.73

31.20 31.20

Number observed to be fluoridated

23.00 18.00

15.00 10.00

16.00 9.00

12.00 4.00

18.00 16.00

34.00 29.00

Difference between observed & expected

+2.50† [0.3049]*

-2.50† [0.3049]*

+2.35† [0.4366]*

-2.65† [0.5551]*

+3.50† [0.9800]*

-3.50† [0.9800]*

+4.00† [2.0000]*

-4.00† [2.0000]*

+1.27† [0.0964]*

-0.73† [0.0319]*

+2.80† [0.2513]*

-2.20† [0.1551]*

Number

expected to be non-fluoridated

3.50 3.50

5.35 5.35

9.50 9.50

7.00 7.00

14.27 14.27

20.80 20.80

Number observed to be non-fluoridated

1.00 6.00

3.00 8.00

6.00 13.00

3.00 11.00

13.00 15.00

18.00 23.00

Difference between observed & expected

-2.50† [1.7857]*

2.50† [1.7857]*

-2.35† [1.0322]*

2.65† [1.3126]*

-3.50† [1.2895]*

3.50† [1.2895]*

-4.00† [2.2857]*

4.00† [2.2857]*

-1.27† [0.1130]*

0.73† [0.0373]*

-2.80† [0.3769]*

2.20† [0.2327]*

>350,000 (C) [48]

200,000– 350,000

(D) [37]

150,000– 200,000

(E) [44]

125,000– 150,000

(F) [30]

100,000– 125,000

(G) [63]

High

*(Observed- Expected) 2/Expected. Total for high crime subgroup 10.9522, low crime subgroup 10.9705, both subgroups χ2 =21.9227

†Comparing the expected and observed numbers of subgroups that were fluoridated. p<0.05, χ2=21.9227, df=11.

Fluoride 2005;38(1)

Water fluoridation and crime in America 17 continuation of this decline at a reduced rate through 1994.16 (See Figure, which plots historical data with solid lines, projects these trends with dashed lines, and compares trends for lead and crime levels, starting with peak numbers for each representing 100% on the same scale.) Lagging the peak and decline of lead levels by about 13 years, violent crime peaked in 1991, and decreased about 30% by 2000.a,17

Blood lead μg/dL 109 4000

US average crime rate per 100,000 population in children aged 1–5 yrs

8 7 3000

15 14 13 12 11

6000 5000

6 5 2000 4 3 2 1 0

0 1976 1980 1984 1988 1992 1996 2000 2004 2008

NHANES NHANES NHANES II III–1 III–2

NHANES = The National Health and Nutrition Examination Surveys Figure. Declines of blood lead and crime

RESULTS

Part A: Media-reported crime database and fluoridation

The carnage for 134 executed events in database “A” includes 325 killed and 224 wounded—about 4.1 casualties per event. b At the midpoint of the period in which these events occurred—March 1997—an estimated 57.5% of the US population was fluoridated. c Of the total of 152 executed and ideational events listed in database “A”, 128 (84.21%) occurred in fluoridated communities or were committed by criminals from fluoridated communities. Of 128 locations

A City Crime Rankings17 shows that crime had hit a similar peak of 5,850 per 100,000 in 1981, dropped to 5038.4 for unclear reasons by 1984, and then increased for 7 years to its 1991 peak of 5,898.4. bThe 1995 bombing of the Federal Building in Oklahoma City is included in database “A”, but the casualties [168 killed, 853 wounded] are not included in this summary, as they would badly skew the portrayal of a typical event. Timothy McVeigh, the convicted bomber, grew up in the fluoridated town of Pendleton, New York, and was stationed at two fluoridated army bases, Fort Benning, GA, and Fort Riley, KS. McVeigh’s remorseless lack of empathy for his victims is believed to exemplify the mental condition of a fluoride-intoxicated killer.

C Data extrapolated/projected from chart and graph, p. xxii- xxiii of Fluoridation Census 1992. US Department of Health and Human Services, Public Health Service, Centers for Disease Control and Prevention, National Center for Prevention Services, Division of Oral Health, Atlanta Georgia 30333. September, 1993. An annual increase in the fluoridated population of 0.4%, from a 12/31/92 level of 55.8%, is projected.

1000

Fluoride 2005;38(1)

18 Seavey related to these events, 98 use silicofluorides, 17 use sodium fluoride, 12 have natural fluoridation, and one combines natural and artificial fluoridation. The average fluoridation level for these 128 communities is 0.983 ppm, and the range is from 0.3 ppm to 4.9 ppm.

Using a population mean of 0.575, a one-sample t test determined the probability of randomly selecting from a 152-count simple random sample (SRS) a sample mean of 0.8421. The null hypothesis, that water fluoridation and these violent crimes vary independently and are unrelated, is rejected (P<0.0005, t=9.001, df=151).18 For database “B”, it was expected that 57.3%, or 94 of the 164 locations identified would be fluoridated. The sample mean was 98 of 164, or 59.8% (one-sample-t-test: P>0.25, t=0.5883, df=163). The chance is thus better than 1 in 4 that the null hypothesis is true, i.e., that fluoridation and gun-based self-defense are randomly associated. So this is a useful control, allowing us to rule out fluoridation-related vagaries of crime reporting or of firearm distribution as a basis for the findings in database “A”. Nevertheless the only valid inference from database “A” concerns the extreme improbability of randomly observing 84.21% fluoridation-related events in a 152-count SRS when only 57.5% were expected.

Crime reporting in the media, and the statistical categorization of crime by the F.B.I., lack at this time a nuanced awareness for identifying “fluoride-related” crime. Whether database “A” demonstrates the objective existence of such a category, or whether it demonstrates that an observer can learn to identify such events from subtle cues found in news stories, it may be seen that both possibilities strongly suggest that such a category exists. The development of database “A” was in any case a necessary step for building a hypothesis of a connection between water fluoridation and crime.

Part B: Online crime database and fluoridation

The six population groupings eliminate city size as a confounding variable, and provide a spread for analyzing variance. Each of the six High Crime subgroups had an average “score” or “crime index” at least 100 points above its corresponding Low Crime subgroup. All six High Crime subgroups had more places fluoridated than expected; all six Low Crime groups had fewer places fluoridated than expected (P<0.05, χ2 = 21.9227 df =11).19 This validates the following preliminary inference: “In American cities having population over 75,000, high crime levels appear to be significantly correlated with water fluoridation.”

Part C: Book crime database and fluoridation

The results are summarized in Table 3. The fluoridation status “Combined”— which is a combination of natural and artificial fluoridation—is an anomaly in having a crime rate 2.9% lower than the non-fluoridated cities.

All of the other types of fluoridation are associated with elevated crime rates. Compared to the crime rate for non-fluoridated cities, natural fluoridation shows a 16.5% higher crime rate; sodium silicofluoride a 37.6% higher crime rate; hydrofluorosilicic acid a 46.8% higher crime rate; and sodium fluoride an 84.9%

Fluoride 2005;38(1)

Water fluoridation and crime in America 19 higher crime rate. Table 3 incorporates population data which are used to convert these elevated crime rates into a putative number of excess crimes associated with water fluoridation in these cities.

Fluoridation statusa

No 122 fluoridation

Combined (natural 12 & artificial)

Natural 18

Sodium silico- 56 fluoride (NaSiF6)

Hydrofluorosilicic 112 acid (H2SiF6)

Sodium fluoride 7 (NaF)

Totals 327 Averages –

Table 3. 327 cities grouped by fluoridation stat

Num- Average ber population

Total population b

Total for 6 major crimes for year 2000

Crime rate, for 6 major crimes, per 100 000 population

Crime rate compared to no fluoridation cities

of cities Excess crimes compared to no fluoridation

cities c

1,813.9 1,760.8 2,112.5 +298.6 +15,322

159,099

443,526

285,077

341,713

257,890

213,962

– 242,756†

19,410,033 352,077 5,322,307 93,715 5,131,391 108,401 19,135,905 477,747 28,883,706 769,289 1,497,736 50,245

79,381,078 1,851,474 – –

0.0 -53.1 -2,826

*The data are from database “327”. aFluoridation data are generally taken from Fluoridation Census 1992 [US Department of Health and Human Services, Public Health Service, Centers for Disease Control and Prevention, National Center for Prevention Services, Division of Oral Health, Atlanta, Georgia 30333, USA; September, 1993] with some corrected and updated information based on telephone inquiries. The category “Other” identified in the Fluoridation Census 1992 has been identified here as “Combined”. bPopulation and crime data are from Morgan KO, and Morgan S, editors, City Crime Rankings, 8th ed. Lawrence, KS: Morgan Quitno Press; 2001. c“Excess Crimes” are calculated by dividing the total population figure on a line by 100,000 and multiplying the result by the crime rate compared to no fluoridation cities on that line. These “excess crimes” are only those for the 327 cities over 75,000 population, totaling 28.5% of the US population. †The total population, 79,381,078, divided by 327, yields the average population per city, 242,755.5902, which is rounded to the nearest whole number. ‡First, the total population, 79,381,078, is divided by 100,000, yielding 793.81078. Second, the total number of crimes, 1,851,474, is divided by this 793.81078, yielding the quotient 2332.387071, which is rounded to two decimal places. This is the average crime rate per 100,000 population for all the 327 cities, including the 122 which are not fluoridated.

2,496.6

2,663.4

3,354.7

– 2,332.39‡

+682.7 +130,640

+849.5 +245,367 +1,540.8 +23,077

– +411,580 – –

0.0

Fluoride 2005;38(1)

20 Seavey Part D: Lead related crime

If we accept the premise that the observed decline in crime is the result of the decline in lead intoxication, we can roughly quantify the amount of crime associated with lead intoxication by comparing the curves for the historical declines in lead and crime, and by projecting them forward from 1993 and 2000, respectively. (See Figure on page 17.)

Projecting the lead level decline on a straight line, it reaches zero by the beginning of 2004. This is an analytically useful end point, even if lead levels will more likely taper off on a curve to a steady state reflecting more or less permanent levels of environmental pollution. The crime decline is projected beyond 2000 along a straight line following its 9-year trend. Note that at the point in time where the straight-line projection for lead reaches zero, the crime rate is still at about 3,365 per 100,000, down from its 1991 peak near 5,900.a

It is thus estimated that by 2004, with blood lead reduced to minimal levels, we will still have 57% of our 1991 peak crime level. It follows that less than half of the 1991 peak level of crime can be attributed to lead intoxication. Alternatively, we would have to hypothesize that relatively low levels of lead generate disproportionately large amounts of crime, and that the relationship between lead levels and crime is extremely non-linear, to a degree that we have seen no reason to suspect.

DISCUSSION

The data show a consistent association between water fluoridation and high crime levels. The traditional socio-cultural determinants of crime—poverty, crowded cities, broken homes, drug use, gangs, and the like—have not been analyzed here as confounding factors, so a causal role for fluorides in crime has not been definitively proven, nor has the role of fluorides been quantitatively established vis-à-vis these other factors. And while conclusions about the statistical significance of findings in Part B remain tentative, all the data nevertheless point in the same disturbing direction, raising serious questions as to whether water fluoridation could possibly be as “safe and effective” as public health authorities and dentists have claimed it to be.

The information on sodium fluoride—despite the small sample—is of particular interest, since sodium fluoride, unlike the silicofluorides, shows little association with elevated blood lead levels.9 It thus appears that sodium fluoride may be associated with crime independently of lead. If sodium fluoride—a salt which dissociates into sodium and fluoride ions in water—is associated with crime independently of a role in the uptake of lead, given that sodium is a normal and well-regulated feature of the human system, it follows that the fluoride ions must be the factor associated with the crime. It then follows that, even in the case of the silicofluorides, the fluoride ions must themselves be contributing to crime

aNote that these rates include larceny and theft, in addition to the six major crimes reported on elsewhere in this paper, so the total rates are higher and cannot be compared to the aggregate rates for the six major crimes reported by MQP.

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Water fluoridation and crime in America 21 independently of silicofluoride’s role in the uptake of lead. Bear in mind that these crime statistics are from the year 2000, when environmental lead had been significantly reduced, and that while the MQP crime data are for the year 2000, the data from the Fluoridation Census are from 1992. The latter are less recent, obviously, but they are the most recent readily available data.

Chemical exposures clearly affect brain function and behavior: lead and mercury are well documented in this regard, and fluorides are gradually becoming better understood. Chemically based crime causality, however, seems to be of a qualitatively different order from the traditionally-accepted types of socio-cultural crime causality. The relationship between these broad categories of causality needs further study, and perhaps a new paradigm is needed to integrate them into a coherent theory.

If the history of lead is any example, however, there may be reason for optimism. Unlike the seemingly intractable socio-cultural determinants, chemical exposures may be amenable to long-term change.

Crime is a measure of social dysfunction, and a barometer for socio-economic dislocation and change. Its causes are infinitely varied in their particulars, nebulous in their totality, and they vary historically from one era to the next. The historical context at any given time, moreover, cannot be duplicated experimentally, challenging the use of scientific methods; and the data that are available to us tend to be colored to some extent by the preoccupations and motives of the era and the people that produced it. There is thus an evident need for an interdisciplinary approach to crime, and for a paradigm which integrates chemistry, statistics, sociology, and history, at a minimum.

The post-Civil War era, for example, saw a significant rise in American crime rates.20 The war may have inured the population to violence; the post-war westward expansion may have created a less-well-ordered frontier society; or those frontiers may have included numerous areas with high fluoride levels in the groundwater—three competing explanations which would doubtless challenge the available data. And while the data in this study focus on the United States during the 1990’s, there are nearby anomalies such as unfluoridated Vancouver, British Columbia., which has experienced high crime rates associated with gangs, drugs, immigration, and ethnic conflict. Immigration, migration, and relocation create difficulties in tracking exposure to fluorides. In the United States, the Clean Air Act (1970) did not address airborne fluorides at all, so we have virtually no data for evaluating exposures from this source.

The senseless multiple shooting became the signature crime of the 1990’s in the United States. Fluoride exposures in many areas may have passed a threshold beyond which “fluoride-related crime” became common. Saturation of Americans with fluorides, via public water supplies, continues to expand. I think we can currently discern the resultant crime effects due to their locational variations. If water fluoridation were ended, it might take a generation for the effects to recede. If it continues to expand, the “signal” identified in this study may get lost in the “noise” of endemic violence.

Fluoride 2005;38(1)

22 Seavey

ACKNOWLEDGEMENT

The author wishes to thank Phyllis Mullenix for pointing out Grandjean’s article. I would also like to thank Prof Burgstahler for his help in organizing this material, and Dr Spittle for his patience in formatting and typesetting it.

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    Published by the International Society for Fluoride Research http://homepages.ihug.co.nz/~spittle/fluoride-journal.htm

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

Fluoride 2005;38(1)

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