RESEARCH PAPERS – A
VITAMIN ‘C’ AND FLUORIDATION
by John A. Yiamouyiannis, Ph.D. (1943-2000)
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.
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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;
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WESTENDORF’S RESEARCH ON
INCOMPLETE DISSOCIATION OF SILICOFLUORIDES
UNDER PHYSIOLOGICAL CONDITIONS
The Kinetics of Acetylcholinesterase Inhibition and the Influence of Fluoride and Fluoride Complexes on the Permeability of Erythrocyte Membranes
Dissertation to receive Ph.D. in Chemistry from the University of Hamburg
By Johannes Westendorf
Hamburg, Germany – 1975
www.fluoridealert.org/westendorf-foreword.htm
Reviewer: Prof Dr. A. Knappwost
Co-Reviewers: Prof, Dr, Malomy Prof, DR, Strehlow Prof, Dr. Hilz Prof Dr. Gercken
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.
Mikecoplan@aol.com Roger.D.Masters@Dartmouth.edu
Foreword by
MJ Coplan and RD Masters, April 2001
.
Westendorf’s 30-year PhD research work is important for reasons beyond its specific scientific findings. First his work was motivated by the assumption that ingested fluoride was beneficial. Knappwost, his thesis supervisor, believed that fluoride in saliva afforded protection against tooth decay and was seeking a means of enhancing the output of fluoride-bearing saliva for that purpose. Therefore, it can hardly be said that Westendorf’s work was biased against water fluoridation.
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 Foreward 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.
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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 compared to control, significant reductions in body weight, feed consumption, absolute uterine weight and number of implantations. Significantly higher incidence of skeletal (wavy ribs, 14th rib, <6 sternal centre, dumbell-shaped second and fifth sternebrae, incomplete ossification of skull and thickening of tibia) and visceral (subcutaneous haemorrhage) abnormalities were also observed in NaF-treated dams than that of control. Oral administration of vitamin C (50 mg/kg body weight) and vitamin E (2 mg/0.2 ml olive oil/animal/day) from day 6 to 19 of gestation along with NaF significantly ameliorates NaF-induced reductions in body weight, feed consumption, absolute uterine weight (only with vitamin E treatment) and number of implantations. As compared with NaF-treated alone, the total percentageof skeletal and visceral abnormalities were significantly lowered in fluoride plus vitamin C-treated animals. Vitamin E was less effective.
These findings suggest that vitamin C significantly reduced the severity and incidence of fluoride-induced embryotoxicity in rats.
Key Words: fluoride • vitamins • embryotoxicity • amelioration
Human & Experimental Toxicology, Vol. 20, No. 12, 619-623 (2001)
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“FLUORIDES, THE DEADLY TOXIN WITHIN”
By 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,
Source: New Sunday Times (Focus) September 2, 2001
The ability of fluoride to reduce thyroid hormone levels has been know for over 100 years (Maumene 1855).
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- New Book-
“THE CASE AGAINST FLUORIDE”

The Case Against Fluoride: How hazardous waste ended up in our drinking water and the bad science and powerful politics that keep it there, by Connett P, Beck J, and Micklem HS, summarizes the historical, political, ethical, toxicological, and epidemiological scientific data behind drinking-water fluoridation.
The book concludes that, if proposed today, fluoridation of drinking water to prevent tooth decay would stand virtually no chance of being adopted, given the current status of scientific knowledge.
In part one of The Case Against Fluoride, “The Ethical and General Arguments Against Fluoridation”: The requirement for the informed consent of the patient before administration of a medication is a basic human right. Yet with fluoride, which is added to drinking water as a therapeutic intervention, no such permission is sought or given. The process is enforced on every member of the population. The authors explore this fact in the context of medical ethics. Another aspect is the efficacy of fluoridation as a therapy, which, the authors argue, is marginal at best and deleterious at worst. The fluoride used for water fluoridation is not of pharmaceutical grade, but is in fact a chemical waste by-product. The lack of any rigorous studies as to the efficacy of fluoridation programs, the authors contend, means that the whole process is experimental.
There is no control of “dose”— how much fluoride anyone receives from the water.
In the case of water fluoridation, according to the above authors, the chemicals that go into the drinking water that more than 180 million people drink each day in the United States are not even pharmaceutical grade, but rather a hazardous waste product of the phosphate fertilizer industry. It is illegal to dump this waste into the sea or local surface water, and yet it is allowed in our drinking water. To make matters worse, this program receives no oversight from the Food and Drug Administration, and the Environmental Protection Agency takes no responsibility for the practice. And from an ethical standpoint, say the authors, water fluoridation is a bad medical practice; individuals are being forced to take medication without their informed consent; there is no control over the dose and no monitoring of possible side effects.
Acute high oral exposure to fluoride may lead to nausea, vomiting, abdominal pain, diarrhea, drowsiness, headaches, polyuria and polydipsia, coma, convulsions, cardiac arrest, and death.
Historically, fluoride was quite expensive for the world’s premier chemical companies to dispose of, but in the 50s and 60s, Alcoa and the entire aluminum industry—with a vast overabundance of the toxic waste—somehow sold the FDA and our government on the insane (but highly profitable) idea of buying this poison and then injecting it into our water supply as well as into the nation’s toothpastes and dental rinses. Consider also that when sodium fluoride is injected into our drinking water, its level is approximately one part-per-million (ppm), but since we only drink one-half of one percent of the total water supply, the hazardous chemical literally “goes down the drain” and voila—the chemical industry not only has a free hazardous waste disposal system, but we have also paid them with our health and our pocketbooks for the process.
The aluminum and phosphate fertilizer industries were not alone. The American government’s atomic weapons program was also producing huge amounts of fluoride and was getting sued by famers for the damage done to their cattle.
.♦.♦.♦.♦.♦.♦.♦.
Evidence Shows Fluoridation Danger
by Paul Connett, PhD
Professor Emeritus of Environmental Chemistry,
St. Lawrence University, Canton, Director of Fluoride Action Network.
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.
The Case Against Fluoride: How hazardous waste ended up in our drinking water and the bad science and powerful politics that keep it there, by Connett P, Beck J, and Micklem HS, summarizes the historical, political, ethical, toxicological, and epidemiological scientific data behind drinking-water fluoridation.
The book concludes that, if proposed today, fluoridation of drinking water to prevent tooth decay would stand virtually no chance of being adopted, given the current status of scientific knowledge.
In part one of The Case Against Fluoride, “The Ethical and General Arguments Against Fluoridation”: The requirement for the informed consent of the patient before administration of a medication is a basic human right. Yet with fluoride, which is added to drinking water as a therapeutic intervention, no such permission is sought or given. The process is enforced on every member of the population. The authors explore this fact in the context of medical ethics. Another aspect is the efficacy of fluoridation as a therapy, which, the authors argue, is marginal at best and deleterious at worst. The fluoride used for water fluoridation is not of pharmaceutical grade, but is in fact a chemical waste by-product. The lack of any rigorous studies as to the efficacy of fluoridation programs, the authors contend, means that the whole process is experimental.
There is no control of “dose”— how much fluoride anyone receives from the water.
In the case of water fluoridation, according to the above authors, the chemicals that go into the drinking water that more than 180 million people drink each day in the United States are not even pharmaceutical grade, but rather a hazardous waste product of the phosphate fertilizer industry. It is illegal to dump this waste into the sea or local surface water, and yet it is allowed in our drinking water. To make matters worse, this program receives no oversight from the Food and Drug Administration, and the Environmental Protection Agency takes no responsibility for the practice. And from an ethical standpoint, say the authors, water fluoridation is a bad medical practice; individuals are being forced to take medication without their informed consent; there is no control over the dose and no monitoring of possible side effects.
Acute high oral exposure to fluoride may lead to nausea, vomiting, abdominal pain, diarrhea, drowsiness, headaches, polyuria and polydipsia, coma, convulsions, cardiac arrest, and death.
Historically, fluoride was quite expensive for the world’s premier chemical companies to dispose of, but in the 50s and 60s, Alcoa and the entire aluminum industry—with a vast overabundance of the toxic waste—somehow sold the FDA and our government on the insane (but highly profitable) idea of buying this poison and then injecting it into our water supply as well as into the nation’s toothpastes and dental rinses. Consider also that when sodium fluoride is injected into our drinking water, its level is approximately one part-per-million (ppm), but since we only drink one-half of one percent of the total water supply, the hazardous chemical literally “goes down the drain” and voila—the chemical industry not only has a free hazardous waste disposal system, but we have also paid them with our health and our pocketbooks for the process.
The aluminum and phosphate fertilizer industries were not alone. The American government’s atomic weapons program was also producing huge amounts of fluoride and was getting sued by famers for the damage done to their cattle.
.♦.♦.♦.♦.♦.♦.♦.
Evidence Shows Fluoridation Danger
by Paul Connett, PhD
Professor Emeritus of Environmental Chemistry,
St. Lawrence University, Canton, Director of Fluoride Action Network.
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.
.♦.♦.♦.♦.♦.♦.♦.
- An Action Web Site ↓
♦.♦.♦.♦.♦.♦.♦.
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