The proper regulation of blood glucose levels is essential to good health. When the body’s ability to regulate blood glucose levels falters, as occurs in diabetes mellitus, chronic elevated glucose levels (hyperglycemia) can lead to serious complications. These consequences include damage to the kidneys, nervous system, cardiovascular system, retina, legs and feet, etc.
As documented by the research cited below, studies on both humans and animals have found that excessive fluoride intake produces an increase in the levels of glucose in blood. In 2006, the National Research Council summarized the available literature as follows:
“The conclusion from the available studies is that sufficient fluoride exposure appears to bring about increases in blood glucose or impaired glucose tolerance in some individuals and to increase the severity of some types of diabetes. In general, impaired glucose metabolism appears to be associated with serum or plasma fluoride concentrations of about 0.1 mg/L or greater in both animals and humans (Rigalli et al. 1990, 1995; Trivedi et al. 1993; de al Sota et al. 1997). In addition, diabetic individuals will often have higher than normal water intake, and consequently, will have higher than normal fluoride intake for a given concentration of fluoride in drinking water. An estimated 16-20 million people in the United States have diabetes mellitus (Brownlee et al. 2002; Buse et al. 2002; American Diabetes Association 2004; Chapter 2); therefore, any role of fluoride exposure in the development of impaired glucose metabolism or diabetes is potentially significant.” (NRC 2006)
Additional research has been published since the NRC’s review in 2006 that further confirms a relationship between fluoride exposure and elevated blood glucose. This research includes a study from China (published in 2000, but not translated into English until 2012), that found high rates of glucose intolerance and diabetes among individuals living in a high-fluoride (8 ppm) area. (Xie 2000) The research also includes studies published prior to 2006 that the NRC did not consider in its review. (e.g., Shahed 1986; Renke 1987).
Although the mechanism by which fluoride increases blood glucose levels is not yet fully understood, it may result in part from fluoride’s affect on the body’s handling of insulin. Insulin is a hormone produced by the pancreas that triggers cells to absorb the glucose circulating in the bloodstream. When the body fails to produce sufficient insulin, or when the cells become desensitized to the insulin that is produced, the body’s ability to clear glucose from the blood becomes impaired. As documented here, studies have found that fluoride can affect both the production of, and sensitivity to, insulin.
Mechanisms Underlying Fluoride-Induced Hyperglycemia
“The mechanism underlying [fluoride-induced] hyperglycemia could include any or all of the following factors: (a) an increase in cellular cAMP followed by an increase in glycogenolysis in fed animals or, in fasted animals, gluconeogenesis; (b) an increase in plasma epinephrine levels; (c) an increase in plasma gluccocorticoid concentrations; and/or (d) a decrease in plasma insulin levels. Additional research is needed to determine which of these possible mechanisms is/are responsible for inducing the observed biochemical changes. ”
SOURCE: Whitford GM, et al. (1987). Topical fluorides: effects on physiologic and biochemical processes. J Dent Res. 66(5):1072-8.
“The fasting blood glucose concentration and the peak value after oral glucose in the exposed group [an endemic fluorosis area with 8 ppm F] were higher than that of the control group [a low fluoride area with <1 ppm F]. The peak value was found 120min after the oral glucose was administered, 60 min later than the peak of the control group. The detectable rates of diabetes and IGT [Impaired Glucose Tolerance] in the exposed group were 11.29% and 20.97% while the rates in the control group were both 0. The detectable rates among patients with severe fluoride bone disease were 22.58% and 35.48%, significantly higher than that of people without the disease (0, 6.5%).”
SOURCE: Xie YP, et al. (2000). Clinical study of the effect of high fluoride on the function of the pancreatic islet b-cells. Chinese Journal of Endemiology 19(2): 84-6.
“Our study has shown for the first time that 40 % of young patients with endemic fluorosis have IGT [impaired glucose tolerance], with elevated serum IRI and low fasting G : I ratios. The serum fluoride levels correlated positively with area under glucose curve in these patients.”
SOURCE: Trivedi N, et al. (1993). Reversible impairment of glucose tolerance in patients with endemic fluorosis. Diabetologia 36: 826-8.
“The data reported in this paper indicate that the transient fluoride increase after an oral dose produces a transitory inhibition of insulin secretion with hyperglycemia as a consequence. . . . The phenomenon was also observed in human beings.”
SOURCE: Rigalli A, et al. (1990). Inhibitory effect of fluoride on the secretion of insulin. Calcif Tissue Int 46:333-8.
“The biggest number of changes which indicate toxic effect of fluorine was found while analyzing sugar curves and phosphorous-calcium-magnesium balance. Six cases of diabetes, 4 of them of early type were diagnosed, mainly in production divisions. On an average, the biggest levels of sugar unfed as well as after administering of glucose, were found at the employees who dispatched superphosphate, then little lower at those who produced fertilizers and phosphoric acid. . . . The number of diabetes cases found is bigger than the average for Polish population . . . . CONCLUSIONS: . . . [Among] the persons with longer period of work the effects of long-lasting influence of fluorine were revealed and were manifested in disturbances of carbohydrates balance with radiographically found thickening of the osseous structure.”
SOURCE: Renke W, et al. (1987). Estimation of occupational hazards of the employees of a phosphate fertilizers plant. Bull. Inst. Mar. Trop. Med. Gdynia 38:5-16.
Exposure to fluoride through drinking water not only significantly increased plasma glucose and lipid profiles, but also elevated both hepatic and renal lipid peroxidation, hepatic lipid profiles and G-6-Pase activity with a reduction in plasma HDL-C, hepatic glycogen content, hexokinase activity and antioxidant status.
SOURCE: Vasant RA, Narasimhacharya AV. (2013). A multigrain protein enriched diet mitigates fluoride toxicity. Journal of Food Science Technology 50(3):528-34.
“Fluoride-exposed rats exhibited significant elevation in fasting blood glucose levels, and the hepatic glycogen content was reduced.”
SOURCE: Vasant RA, Narasimhacharya AVRL. (2012). Ameliorative effect of tamarind leaf on fluoride-induced metabolic alterations. Environ Health Prev Med. DOI 10.1007/s12199-012-0277-7
“The present study also confirms earlier findings that, when the diabetic animals are exposed to F, a further increase in plasma glucose levels and a decrease in hepatic glycogen content occur.”
SOURCE: Vasant RA, et al. (2010). Therapeutic benefits of glibenclamide in fluoride intoxicated diabetic rats. Fluoride 43(2): 141-9.
“The F group experienced higher significant increases in serum glucose concentration than those of control mice at 60, 90, 120 and 240min after administration of glucose. The differential analysis of the AUC of the response obtained with the [oral glucose tolerance test] shows a significant increase of 22.8% in the F exposed group.”
SOURCE: Garcia-Montalvo EA, et al. (2009). Fluoride exposure impairs glucose tolerance via decreased insulin expression and oxidative stress. Toxicology 263: 75-83.
“In the glycemia comparison at each period of time, the group treated with NaF showed significantly higher glycemia compared with the control group”
SOURCE: Chehoud KA, et al. (2008). Effects of fluoride intake on insulin sensitivity and insulin signal transduction. Fluoride 41(4): 270-5.
“In our experiment, we found a statistically insignificant increase of glucose concentration in blood serum, by 12% (group with F–) and by 17% (group with F– + caffeine). The increase of glucose concentration influenced by F– is known. It is connected with the concentration of NaF administered, although even with low doses of F– the concentration of glucose in serum might increase. It is probable that fluorides intensify the glucogenetic processes.”
SOURCE: Birkner E, et al. (2006). Influence of sodium fluoride and caffeine on the concentration of fluoride ions, glucose, and urea in blood serum and activity of protein metabolism enzymes in rat liver. Biol Trace Elem Res. 112(2):169-74.
“The study was done in 30 one-month-old Wistar FL rats divided into one control and two study groups of ten animals each. Hyperglycemia was induced with sodium fluoride in water at a concentration of 50 or 100 mg/L during four months.”
SOURCE: Grucka-Mamczar E, et al. (2004). [Activities of some enzymes and concentration of ammonia in serum of rats with fluoride hyperglycemia]. [Article in Polish]. Ann Acad Med Stetin. 50 Suppl 1:36-41.
“[S]erum concentrations of glucose and fluoride rose significantly in exposed rats. Rats exposed to 50 mg F-/L showed an increase in the mean glucose level of 60% in comparison to controls. Fluoride levels increased 3.5 times in this group. With higher concentration of fluoride in drinking water (100 mg F-/L) the increase in glucose level was 78%. Fluoride levels were increased 6 times compared to the control value.”
SOURCE: Chlubek D, et al. (2003). Activity of pancreatic antioxidative enzymes and malondialdehyde concentrations in rats with hyperglycemia caused by fluoride intoxication. J. Trace Elem. Med. Biol. 17:57-60.
“The blood glucose fasting concentrations significantly increased in diabetic groups. Hyperglycemia was manifested more in DF10 [diabetic rats exposed to 10 ppm F in drinking water for 3 weeks] than in D [diabetic rats exposed to 0 ppm F in drinking water for 3 weeks].”
SOURCE: Boros I, et al. (1998). Fluoride intake, distribution, and bone content in diabetic rats consuming fluoridated drinking water. Fluoride 31(1):33-42.
“Intraperitonial administration of 10 mg fluoride (NaF)/kg body weight resulted in hyperglycemia in rats. Role of gluconeogenesis and glycogenolysis in this hyperglycemic response was evaluated. Results of the study indicate that the fluoride induced hyperglycemia is mainly due to increased hepatic glycogenolysis.”
SOURCE: Varadacharyulu NC, Rao PR. (1997). Gluconeogenesis and glycogenolysis in fluoride-treated rats. Indian Journal of Experimental Biology 35(8):906-8.
“Present experiments indicate that chronic fluoride administration at low rates of intake and absorption produce a subtle disturbance of glucose tolerance that can be made evident by means of glucose tolerance tests.”
SOURCE: Rigalli A, et al. (1992). Bone mass increase and glucose tolerance in rats chronically treated with sodium fluoride. Bone & Mineral 16:101-08.
“The oral administration of sodium fluoride (NaF) (40 umol/100 g body weight) to fasting rats produced an immediate fall in insulin levels and the consequent increase in glycemia. These phenomena were observed with plasma fluoride concentrations 5-15 uM. . . . The phenomenon could be reproduced after consecutive doses of fluoride, with successively increasing hyperglycemia responses.”
SOURCE: Rigalli A, et al. (1990). Inhibitory effect of fluoride on the secretion of insulin. Calcif Tissue Int 46:333-8.
“There was a significant increase in serum glucose (120% increase), and serum fluoride (10 to 700 fold) 30 min after the injection of NaF. . . . It is concluded that the NaF induced hyperglycemia could be due in part to the reduction of serum insulin which would decrease the uptake of glucose by muscle and adipose. It should be noted that the lowest dose of NaF (0.5 mg/kg) is in the range of fluoride ingestion observed following a topical application of APF gel. Thus it is conceivable that normal ingestion of F following an APF application could alter several metabolic processes.”
SOURCE: Shahed AR, et al. (1986). Effect of F on rat serum insulin levels in vivo. Journal of Dental Research 65:756.
“In the present study, we found that serum glucose increased immediately after a single large dose of fluoride (NaF 35 mg/kg, ip).”
SOURCE: Suketa Y, Asao Y, Kanamoto Y, et al. (1985). Changes in adrenal function as a possible mechanism for elevation of serum glucose by a single large dose of fluoride. Tox Appl Pharm 80: 199-205.