— VITAMIN C AND FLUORIDATION —
by John A. Yiamouyiannis, Ph.D. (1943-2000)
The National Health Federation
P.O. Box 688, Monrovia, California 91017
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.
- 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.
(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. 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;
(21) Hardwick & Bunting, J. Dent. Res. 50 (Supplement, Pt. 1), 1212 (1971)