It has been known since the 1930s that poor nutrition enhances the toxicity of fluoride. As discussed below, nutrient deficiencies have been specifically linked to increased susceptibility to fluoride-induced tooth damage (dental fluorosis), bone damage (osteomalacia), neurotoxicity (reduced intelligence), and mutagenicity. The nutrients of primary importance appear to be calcium, vitamin C, and iodine, while magnesium, vitamin D, and protein appear to be important as well.

With respect to the teeth, the severity of dental fluorosis has been found to correlate with decreased calcium intake. Thus, a child consuming inadequate calcium can develop dental fluorosis at a dose that will not effect a child with adequate calcium. As noted in the Journal of the American Dental Association in 1952:

“The data from this and other investigations suggest that malnourished infants and children, especially if deficient in calcium intake, may suffer from the effects of water containing fluorine while healthy children would remain unaffected…Thus low levels of fluoride ingestion which are generally considered to be safe for the general population may not be safe for malnourished infants and children. Therefore, the nutritional status must be carefully assessed and guarded in areas with endemic fluorosis. Nutritional studies should be included in any comprehensive program of fluoridation of water with special attention to chronically ailing infants and children…When an individual or a population group shows mottling beyond the degree expected, the health and nutritional status of that group should be investigated.”
SOURCE: Massler M, Schour I. (1952). Relation of endemic dental fluorosis to malnutrition. JADA. 44: 156-165.

Similarly, research has found that inadequate intake of calcium renders the skeleton more susceptible to fluoride-induced osteomalacia. As noted by the National Research Council of Canada:

“There is . . . definite evidence that fluoride supplementation creates a greater metabolic requirement for calcium in humans. Much of this evidence has accrued from attempts to treat human osteoporosis by means of high doses of fluoride. . . . If the calcium insufficiency is not corrected, fluoride supplementation can induce osteomalacia.  Jowsey et al. have stated that “osteomalacia and secondary hyperparathyroidism observed in previous studies were caused by fluoride and a calcium intake insufficient to mineralize the new bone… Kyle et al. commented that “in the absence of additional calcium, the bone is incompletely mineralized. If fluoride administration continues … the net result will be osteomalacia and increased bone resorption.” To prevent osteomalacia, the calcium supplement must be “administered concurrently” with fluoride. Jowsey and Kyle recommend that, in high-fluoride therapy, the calcium supplements, given concomitantly, should be 35 to 40 times the fluoride supplement, by weight. . . . If this same fluoride-to-calcium proportionality applies to chronic daily intake of fluoride, then the ingestion of 5 mg of fluoride per day would require a supplemental intake of 200 mg calcium per day.”
SOURCE: Marier J, Rose D. 1977. Environmental Fluoride. National Research Council of Canada. Associate Committe on Scientific Criteria for Environmental Quality. NRCC No. 16081.

With respect to neurotoxicity, both animal and human studies have found that fluoride exacerbates the neurological effects of iodine deficiency. (Hong 2001; Lin Fa-Fu 1991; Guan 1988). As noted by Hong:

“When high fluoride and low iodine co-occur there appear to be compounding effects on the population in endemic areas with a negative influence on child intellectual development that is more pronounced than the case of low iodine alone.”
SOURCE: Hong F, et al. (2001). Research on the effects of fluoride on child intellectual development under different environments. Chinese Primary Health Care 15(3):56-7. [Republished in Fluoride 2008; 41(2):156–60.]

Finally, research dating back to the 1940s has found that deficiencies of vitamin C enhance the skeletal effects of fluoride exposure. As noted by a team of Indian scientists in 1940:

“The incidence and severity of the disease [skeletal fluorosis] had a definite relation to the economic and nutritional status of the communities… A pronounced deficiency of the vitamin C factor in the diet was especially associated with a severe incidence of the disease.”
SOURCE: Pandit CG, et al. (1940). Endemic fluorosis in South India. Indian Journal of Medical Research 28: 533-558.

Based on subsequent animal and human research, the National Research Council of Canada stated: “It appears possible that chronic exposure to fluoride increases the metabolic requirement for vitamin C.” (NRCC 1977). Consistent with this observation, a voluminous body of recent research has found that fluoride increases oxidative stress and that a diet rich in anti-oxidants (including vitamin C) ameliorates fluoride’s toxicity. A diet poor in vitamin C and/or anti-oxidants will thus greatly increase an individual’s susceptibility to fluoride.

Nutritional Deficiencies Enhance Fluoride’s dangers

“the results of the present study indicate that both a multigrain diet rich in nutrients and antioxidants, and fortified with protein is useful in mitigating the fluoride toxicity.”
SOURCE: Vasant RA, Narasimhacharya AV. (2013). A multigrain protein enriched diet mitigates fluoride toxicity. Journal of Food Science Technology 50(3):528-34.

“Poor nutrition increases the incidence and severity of dental fluorosis and skeletal fluorosis.”
SOURCE: Agency for Toxic Substances & Disease Registry (ATSDR) (2003). Toxicological profile for fluorides, hydrogen fluoride, and fluorine. Atlanta, GA: U.S. Department of Health and Human Services, Public Health Service.

“Risk and severity of [skeletal fluorosis] seem inversely related to calcium intake . . . .”
SOURCE: Whyte MP, et al. (2008). Skeletal fluorosis from instant tea. J Bone Miner Res. 23(5):759-69.

“These findings indicate that adequate of supplementary ingestion of dietary factors such as protein or calcium may significantly reduce toxic effects of fluoride on bone.”
SOURCE: He Y, et al. (2008). Effects of protein versus calcium supplementation on bone metabolism and development in fluoride-exposed offspring rats fed protein- and calcium-deficient diets. Fluoride 41:192-98.

“These results indicate that calcium prevents not only fluoride-induced hypocalcemia but also the locomotor behavioral and dental toxicities of fluorideby decreasing bioavailability of fluoride.”
SOURCE: Ekambaram P, Paul V. (2001). Calcium preventing locomotor behavioral and dental toxicities of fluoride by decreasing serum fluoride level in rats. Environ Toxicol Pharmacol. 9(4):141-146.

“Protein deficiency . . . aggravates fluoride toxicity. A protein-supplemented diet might therefore substantially mitigate certain fluoride-induced health hazards in humans living in endemic areas.”
SOURCE: Chinoy NJ, Mehta D. (1999). Effects of protein supplementation and deficiency on fluoride-induced toxicity in reproductive organs of male mice. Fluoride 32: 204-214.

“With increasing food calcium ingestion during the development of teeth, the level of dental fluorosis is decreasing. The calcium supply is effective in protection from fluoride toxicity to a certain extent.”
SOURCE: Ouyang W, et al. (2000). [Effect caused by uptake of different levels of calcium to enamel fluorosis in rats] [Article in Chinese]. Zhonghua Kou Qiang Yi Xue Za Zhi. 35(1):47-9.

“[M]alnourished individuals appear to be more prone to develop dental and skeletal fluorosis.”
SOURCE: Littleton J. (1999). Paleopathology of skeletal fluorosis. American Journal of Physical Anthropology 109: 465-483.

“In calcium-deficient children the toxic effects of fluoride mainfest even at marginaly high (>2.5 mg/d) exposures to fluoride.”
SOURCE: Teotia M, Teotia SP, Singh KP. (1998). Endemic chronic fluoride toxicity and dietary calcium deficiency interaction syndromes of metabolic bone disease and deformities in India: year 2000. Indian Journal of Pediatrics 65:371-81.

“The basic effect of excess fluoride on bone is the causation of a high bone turnover state which can also be induced to a milder extent by low calcium diet itself. Therefore, the formation of a high bone turnover state is the pathogenetic basis for low dietary calcium intake to exacerbate the severity of skeletal fluorosis.”
SOURCE: Li G, Ren L. (1997). [Effects of excess fluoride on bone turnover under conditions of diet with different calcium contents]. [Article in Chinese]. Zhonghua Bing Li Xue Za Zhi. 26(5):277-80.

“It was also evident that the osteopenic radiological picture [of fluorosis] is more commonly found in the poorer and undernourished population of the village.”
SOURCE: Mithal A, et al. (1993). Radiological spectrum of endemic fluorosis: relationship with calcium intake. Skeletal Radiology 22: 257-61.

“The significant differences in IQ among these regions suggests that fluoride can exacerbate central nervous lesions and somatic developmental disturbance caused by iodine deficiency.”
SOURCE: Lin Fa-Fu, et al (1991). The relationship of a low-iodine and high-fluoride environment to subclinical cretinism in Xinjiang. Iodine Deficiency Disorder Newsletter. 7(3):24-25.

“Diets high in fat have been reported to increase deposition of fluoride in bone and, thus, to enhance toxicity.”
SOURCE: Department of Health & Human Services. (U.S. DHHS) (1991). Review of Fluoride: Benefits and Risks. Report of the Ad Hoc Committee on Fluoride, Committee to Coordinate Environmental Health and Related Programs. Department of Health and Human Services, USA.

“As reported for dental fluorosis the modifications in bone tissue histology caused by high fluoride intake could be mitigated by the influence of dietary factors.”
SOURCE: Boivin G, et al. (1989). Skeletal fluorosis: histomorphometric analysis of bone changes and bone fluoride content in 29 patients. Bone 10:89-99.

“Additional factors thought to contribute to development of endemic fluorosis include calcium deficiency and poor nutrition.”
SOURCE: Fisher RL, et al. (1989). Endemic fluorosis with spinal cord compression. A case report and review. Archives of Internal Medicine 149: 697-700.

“In conclusion, it appears that the degree of hypocalcemia (possibly due to low dietary calcium intakes) plays a major role in determining the severity of osteomalacia present in endemic skeletal fluorosis.”
SOURCE: Pettifor JM, et al. (1989). Endemic skeletal fluorosis in children: hypocalcemia and the presence of renal resistance to parathyroid hormone. Bone Miner. 7(3):275-88.

“The study suggests that there is synergistic action of iodine-deficiency and fluorine-intoxication on the thyroid.”
SOURCE: Guan ZZ, et al. (1988).  Synergistic action of iodine-deficiency and fluorine-intoxication on rat thyroid. Chin Med J (Engl). 101(9):679-84.

“The test animals were fed with low-grade food during 2-5 months under conditions of acute and chronic action of hydrogen phosphide and hydrogen fluoride induced by inhalation, that resulted in the pronounced impairment of the chromosomal apparatus of the bone marrow cells in the rats. A principal possibility has been established of modification of the hydrogen phosphide and hydrogen fluoride cytogenetic effect by the alimentary action. In particular, it has been found that the effect is significantly higher when the rats are fed with a low-grade ration than under conditions of balanced nutrition.”
SOURCE: Tazhibaev ShS, et al. (1987). [Modifying effect of nutrition on the mutagenic activity of phosphorus and fluorine compounds]. Vopr Pitan. (4):63-6.

“substantial fluoride intake may magnify the need for adequate dietary calcium and vitamin D intake, particularly in premenopausal women.”
SOURCE: Sowers MR, et al. (1986). The relationship of bone mass and fracture history to fluoride and calcium intake: a study of three communities. Am J Clin Nutr. 44(6):889-98.

“Community based studies strongly suggest that calcium status modifies the type of bone changes seen in fluorosis.”
SOURCE: Krishnamachari KA. (1986). Skeletal fluorosis in humans: a review of recent progress in the understanding of the disease. Progress in Food and Nutrition Sciences 10(3-4):279-314.

“Clinical and radiological profiles of the patients revealed that they were from suffering dental and skeletal fluorosis. Several factors appear important in affecting the degree of severity, including nutritional status . . . . [T]he relief was greatest among those receiving nutritional supplements in addition to defluoridated water.”
SOURCE: Rayjalakashmi K, et al. (1986). Investigations on the Relevance of Defluoridated Water and Nutritional Supplements in Fluorosis Endemic Areas in Andhra Pradesh, India. Studies in Environmental Science 27:357-67.

“Over 90% of the persons affected with severe skeletal fluorosis, bone disease and deformities belong to the low socio-economic group of the farming community and they had generalized nutritional deficiencies.”
SOURCE: Teotia SPS, et al. (1984). Environmental fluoride and metabolic bone disease: an epidemiological study (fluoride and nutrient interactions). Fluoride 17: 14-22.

“The beneficial effects of calcium and magnesium in alleviating fluorosis has been confirmed in animal studies. Low-calcium diets increased bone fluoride in rats (Guggenheim et al. 1976), increased the severity of bone fluorosis, with “exostosis” lumps, in rabbits (Reddy and Rao 1972b), and increased bone fluoride and the severity of its effects in monkeys (Reddy and Srikantia 1971). Conversely, high dietary calcium and phosphorus lowered bone fluoride in swine (Forsyth et al. 1972), and calcium supplementation decreased the lesions of fluorosis in cows, horses, and swine (Spencer, Cohen and Garner 1974).”
SOURCE: Marier J, Rose D. 1977. Environmental Fluoride. National Research Council of Canada. Associate Committe on Scientific Criteria for Environmental Quality. NRCC No. 16081.

“Unlike most species, primates cannot synthesize their own vitamin C, and are entirely dependent on their food-chain to supply an adequate intake. In a study of fluoride supplementation in monkeys, Reddy and Srikanti (1971) showed that a diet low in vitamin C enhanced the onset of skeletal fluorosis, and that a low protein intake accelerated rarefaction of bones. Earlier, Gabovich and Maistruk (1963) had shown that vitamin C supplementation reduced the toxic effects of fluoride in industrial workers and in Guinea pigs. Marier and Rose (1971) discussed Russian studies in which fluorosis was found to be most severe in children who had a vitamin C deficiency. Marier and Rose also discussed Australian work, which showed that vitamin C supplementation alleviated fluorosis in Guinea pigs. It appears possible that chronic exposure to fluoride increases the metabolic requirement for vitamin C,  but again, such nutritional interrelations have not yet been quantified.
SOURCE: Marier J, Rose D. 1977. Environmental Fluoride. National Research Council of Canada. Associate Committe on Scientific Criteria for Environmental Quality. NRCC No. 16081.

“The occurrence of this syndrome among the poorer segments of the populations is suggestive of a detrimental role of undernutrition on fluoride-induced toxicity.”
SOURCE: Krishnamachari KA, Krishnaswamy K. (1973). Genu valgum and osteoporosis in an area of endemic fluorosis. The Lancet 2: 877-879.

“Evidence of malnutrition in fluorosis-prone subjects has been cited by several investigators. Therefore, it is reasonable to suggest that subjects suffering from dietary deficiencies or metabolic malfunction may have an increased susceptibility to fluorosis.”
SOURCE: Marier JR, et al. (1963). Accumulation of skeletal fluoride and its implications. Archives of Environmental Health 664-671.

“The data from this and other investigations suggest that malnourished infants and children, especially if deficient in calcium intake, may suffer from the effects of water containing fluorine while healthy children would remain unaffected…Thus low levels of fluoride ingestion which are generally considered to be safe for the general population may not be safe for malnourished infants and children. Therefore, the nutritional status must be carefully assessed and guarded in areas with endemic fluorosis. Nutritional studies should be included in any comprehensive program of fluoridation of water with special attention to chronically ailing infants and children…When an individual or a population group shows mottling beyond the degree expected, the health and nutritional status of that group should be investigated.”
SOURCE: Massler M, Schour I. (1952). Relation of endemic dental fluorosis to malnutrition. JADA. 44: 156-165.

“there seemed to be a definite connection between the development of joint symptoms and poverty or intercurrent infections, since the disease appeared to be much more severe in those who had the least opportunity for healthy living.”
SOURCE: Kilborn LG, et al. (1950). Fluorosis with report of an advanced case. Canadian Medical Association Journal 62: 135-141.

“The incidence and severity of the disease had a definite relation to the economic and nutritional status of the communities… A pronounced deficiency of the vitamin C factor in the diet was especially associated with a severe incidence of the disease.”
SOURCE: Pandit CG, et al. (1940). Endemic fluorosis in South India. Indian Journal of Medical Research 28: 533-558.

“It has been suggested by some authorities investigating this condition that a low calcium intake hastens the onset and development of this chronic fluorine poisoning. In other words a high fluorine intake on a normal consumption of calcium in the diet will produce the condition as well as a comparatively low calcium intake in the diet. In view of this evidence that a diet high in calcium tends to offset the defects of fluorine it would seem feasible that as a protective measure for children living in the endemic [fluorosis] areas and questionable areas to partake of a diet relatively high in calcium content.”
SOURCE: Blue JA. (1938). Mottled enamel in Oklahoma Panhandle, and its possible relations to child development. Journal of the Oklahoma State Medical Association 31:295-301.

“A diet rich in Ca, P, and vitamin D has an influence on the course of the intoxication, but does not prevent its occurrence.”
SOURCE: Roholm K. (1937). Fluoride intoxication: a clinical-hygienic study with a review of the literature and some experimental investigations. London: H.K. Lewis Ltd.

“In a region where there is a possibility of ingesting fluorine in toxic quantities, there will be individuals who ingest it without giving clinical symptoms of intoxication. Cristiani has applied the term latent fluorine intoxication to this condition. The manifest intoxication symptoms then develop if the fluorine intake is raised or the sensibility to fluorine increases for some reason (Ca or vitamin deficiency, etc). This explains why bones and teeth sometimes contain the same quantity of fluorine in apparently healthy individuals as in individuals with definite symptoms of intoxication.”
SOURCE: Roholm K. (1937). Fluoride intoxication: a clinical-hygienic study with a review of the literature and some experimental investigations. London: H.K. Lewis Ltd.