New scientific research on fluoride toxicity further highlights the misguided emphasis of most fluoride research in the US. Whereas the vast majority of fluoride studies in the US continue to focus exclusively on fluoride’s impact on teeth, the research identified below shows that fluoride’s impact on health extends well beyond the shiny, or mottled, surface of the tooth.

Listed below are recent studies investigating the relationship between silicofluorides and blood lead levels in children, studies investigating the interactive effects of fluoride and iodine, and studies investigating the impact of fluoride on thyroid, brain, insulin secretion, skeletal health, and the kidney.

We start first, however, with a new study bringing into question the purported effectiveness of water fluoridation in preventing cavities.

FLUORIDE & TOOTH DECAY

STUDY: Meyer-Lueckel H, et al. (2006). Caries and fluorosis in 6- and 9-year-old children residing in three communities in Iran. Community Dentistry and Oral Epidemiology 34:63-70.

“In the present study, fluoridated water did not seem to have a positive effect on dental health, as it might have been expected in a community with the respective caries prevalence.”

COMMENTARY: This study is the latest among a growing number of studies which call into question the effectiveness of water fluoridation. When this German research team studied the teeth of randomly selected children from 3 Iranian communities, they were unable to find a correlation between the fluoride content of water (0.2 ppm, 0.3 ppm, and 1.3 ppm) and the children’s cavity experience.

If there is a weakness to this study, however, it is that the authors did not control for the impact of income – a limitation which the authors readily acknowledge and discuss. It is interesting to note, in this context, the study by Colquhoun (1985), which found that — if income levels are carefully accounted for (a rarity in fluoridation research) — there is no difference in cavity rates between fluoridated and unfluoridated areas. To read Colquhoun’s study, see: http://www.fluoridealert.org/health/teeth/caries/colquhoun-1985.pdf

SILICOFLUORIDES AND BLOOD LEAD

STUDY: Macek M, et al. (2006). Blood lead concentrations in children and method of water fluoridation in the United States, 1988-1994. Environmental Health Perspectives 114:130-134.

COMMENTARY: This study, co-authored by 2 scientists from the Centers for Disease Control (CDC), attempted to replicate the findings of Masters & Coplan (1999, 2000) on the relationship between water fluoridation and lead levels in children’s blood. While the authors conclude that their findings “do not support concerns that silicofluorides in community water systems cause higher PbB [lead] concentrations in children” their study is by no means a clean refutation of Masters and Coplan’s work. Indeed, the authors acknowledge that water fluoridation may be associated with increased increased lead levels among children living in houses built prior to 1946, and in houses of “unknown age”. To quote:

“Controlling for covariates, water fluoridation method was significant only in the models that included dwellings built before 1946 and dwellings of unknown age.”

Coming from a team of CDC scientists, with a strong institutional bias in favor of fluoridation, I find this result to be quite interesting and intriguing. After all, there is no short supply of houses built prior to 1946.

Here’s a more nuanced description of the authors’ findings:

“fluoridation was significantly associated with PbB [lead] concentration only for the “before 1946” (adjusted Wald-F= 2.8; p= 0.03) and “unknown” (adjusted Wald-F= 2.8; p= 0.03) strata. In the before-1946 model, however, none of the individual fluoridation categories (including the silicofluorides compounds) was significantly higher than the reference no-fluoride category. In the unknown-year model, the hydrofluosilicic acid category was significantly different than the no-fluoride category: the GM PbB concentration for hydrofluosilicic acid was 45% higher. This significant association between hydrofluosilicic acid and GM PbB concentration seen in the unknown-year stratum was not observed in the other strata. In addition, there was no trend toward increasing GM ratios for the silicofluoride categories with increasing dwelling age.”

I look forward to hearing Roger Masters’ & Mike Coplan’s comments and analysis of this study.

FLUORIDE & INSULIN SECRETION

STUDY: Menoyo I et al. (2005). Effect of fluoride on the secretion of insulin in the rat. Arzneimittelforschung 55:455-60.

COMMENTARY: This study is the latest in a series of studies from an Argentinian research team (Rigalli et al). Their research is nothing short of fascinating. In animal studies, human studies, and in-vitro laboratory studies, they have shown that fluoride inhibits the secretion of insulin – and at notably low concentrations. For instance, the authors have repeatedly found that fluoride at a concentration of just 95 parts per billion (ppb), or 5 umol/L, significantly inhibits the secretion of insulin. This concentration of fluoride is lower than the peak blood fluoride concentrations following ingestion of some fluoridated dental products, and lower than the blood fluoride concentrations found in some individuals with kidney disease, heart disease, osteoporosis, and combinations thereof.

The potential implications of this research (e.g. implications for diabetes prevalence/severity?) is not yet known, but certainly worthy of consideration – particularly since at least one of the authors’ studies (Rigalli 1995) found a suggestive effect of fluoride on insulin secretion at a concentration as low as 38 parts per billion (a blood fluoride concentration that many people in fluoridated and unfluoridated areas will attain).

The authors’ summarize their findings as follows:

“We have shown that 1 h after the intake of 1.44 mmol (60 mg) of NaF by fasting human volunteers, plasma fluoride increased up to 15 umol/L and insulin levels decreased significantly [1]. The same phenomenon was reproduced in rats. The oral administration of sodium fluoride [40 umol/100 g body weight) to fasting rats produced an immediate increase in plasma fluoride, a fall in insulin levels and the consequent increase in glycemia. With the washing-out of fluoride from plasma and soft tissues (4-5 h), glycemia and insulin returned to normal levels. The insulin secretion of isolated Langerhans islets perfused with solutions containing 5-20 umol/L fluoride was found significantly inhibited as a function of fluoride levels, both with basal and stimulatory concentrations of glucose [1]. In agreement, we have reported that in a group of 24 women and two men (44-66 years old, ex-residents of an area of endemic fluorosis) with fasting fluoremias of 0.5 to 9.2 umol/L, the area under the curve (AUC) of insulin during standard glucose tolerance tests showed an inverse relationship with fluoremia [2]. The overall information afforded by present experiments indicate that extracellular concentrations of fluoride above 5 umol/L [95 parts per billion] affect the insulin excretion. The results suggest that fluoride affects some stage of insulin secretion situated below the cascade of events that include the participation of calmodulin, protein-kinase C and cyclic AMP.”

FLUORIDE & IODINE INTERACTIONS: IMPACT ON THYROID & BRAIN

COMMENTARY: In reviewing the scientific literature on fluoride, I have become particularly compelled by evidence indicating that a deficiency of iodine can exacerbate the toxicity of fluoride – and vice versa (Guan 1988; Lin 1991; Zhao 1998). With the CDC recently reporting that 12% of Americans have some degree of iodine deficiency, the interactive effects of fluoride and iodine is a health issue that demands much greater attention.

However, while Chinese research indicates that fluoride concentrations as low as 0.91 ppm can increase the neurological deficits of iodine deficiency in children (Lin 1991), virtually NO research on this issue has yet been conducted by American scientists. Instead, fluoride research in the U.S. continues to be dominated by the National Institute of Dental and Craniofacial Research (NIDCR) and their near exclusive focus on teeth.

Here are five new studies (2 human, and 3 animal) that add yet further concern that fluoride exposure can worsen the impact of low iodine and vice versa.

STUDY: Anon. (2005). [The specific features of the development of iodine deficiencies in children living under environmental pollution with fluorine compounds] Gigiena i sanitariiaNov-Dec(6):53-5.

“Natural iodine deficiency and ambient air pollution with fluorine compounds were examined for their combined influence on the prevalence and severity of iodine-deficiency disorders. The excess intake of fluorine was shown to increase the incidence of thyroid diseases and to lower anthropometric indices in children. The preventive measures performed to eliminate iodine-deficiency disorders under intensive ambient air pollution with fluorine compounds were found to be insufficiently effective.”

STUDY: Ruiz-Payan A, Duarte-Gardea M, Ortiz M, Hurtado R (2005). Chronic effects of fluoride on growth, blood chemistry, and thyroid hormones in adolescents residing in northern Mexico. Paper presented at the XXVIth Conference of the International Society for Fluoride Research. September 26-29. Fluoride 38: 46.

“This study was designed to evaluate adverse health effects in adolescents from chronic exposure to various water fluoride concentrations in three communities located in northern Mexico: Ciudad Juarez, Samalayuca, and Villa Ahumada. In these communities the fluoride concentration in water averages 0.3, 1.0, and 5.3 mg/L, respectively. The residents of Villa Ahumada have been exposed to excessive levels of fluoride in drinking water since their birth. Using urinary fluoride as biomarker, we evaluated the effect of fluoride on dental fluorosis, growth, thyroid hormones, hepatic function, lipids, uric acid, and electrolytes. A total of 201 adolescents (106 female, 95 male), aged 15–20, were included in the study… In Villa Ahumada 97 percent of all adolescents exhibited dental fluorosis, and 18 percent of them have serious damage to their teeth. In Samalayuca 53 percent of all adolescents exhibited mild dental fluorosis, 15 percent of them have moderate dental fluorosis, and 2 percent showed serious damage in their teeth. In Villa Ahumada a significant inverse relationship was found between urine fluoride levels and stature; this association suggests that fluoride exposure may affect the teeth but also the growth of adolescents. Serum samples of these individuals showed elevated levels of alkaline phosphatase (ALP), potassium, magnesium, calcium, and phosphate, and decreased levels of thyroid hormone T3 and uric acid. These findings show that high fluoride ingestion has a definite relationship with the prevalence and severity of dental fluorosis, decrease of stature, and decrease of thyroid hormone secretion. Uric acid is one of the important antioxidants of plasma, and its level was lower in fluorotic adolescents, indicating that fluoride toxicity may involve a reduction on certain intrinsic scavengers resulting in an increased vulnerability to oxygen free radical toxicity.”

STUDY: Ge Y, et al. (2005). DNA damage in thyroid gland cells of rats exposed to long-term intake of high fluoride and low iodine. Fluoride 38: 318-323.

“SUMMARY: Thirty-two one-month-old Wistar albino rats were divided randomly into four equal groups of eight (female:male = 3:1). To assess damage to DNA in their thyroid gland cells, the first group (1) of rats served as the untreated control, the second group (2) was administered a high concentration of fluoride (HiF, 100 mg NaF/ L [45 mg F–/L] in their drinking water), the third group (3) was placed on a low iodine intake (LI, 0.0855 mg I/kg diet), and the fourth group (4) was exposed to the high fluoride and low iodine treatment combined (HiF+LI). At 20 months of age, the rats were sacrificed for experimental purpose and their thyroid gland cells were removed for single cell gel electrophoresis (SCGE = comet assay). In comparison with DNA damage in the thyroid gland cells of the control group 1 (10.74 ± 12.59%), such DNA damage in the LI, HiF, and HiF+LI groups 2, 3, and 4, was 83.50 ± 10.20%, 83.03 ± 12.11%, and 89.32 ± 8.21%, respectively. Moreover, the proportion of grade III thyroid gland cell damage increased by 32.26% in group 2, 47.83% in group 3, and 69.23% in group 4, as compared to the control group 1. These findings indicate that excessive long-term intake of fluoride, with or without adequate I intake, is a significant risk factor for the development of thyroid dysfunction.”

STUDY: Ge Y, et al. (2005). Effects of high fluoride and low iodine on brain histopathology in offspring rats. Fluoride 38: 127-132.

“SUMMARY: Thirty-two Wistar rats were divided randomly into four groups of six females and two males each. The experimental groups were exposed to high fluoride drinking water (45 mg F–/L from 100 mg NaF/L), low dietary iodine (0.0855 mg/kg), or both together in order to assess the effects of these three factors on the structure of the brain of the offspring rats. After the animal model was established, offspring rats were bred, and thirty-six rats from each group (female:male = 1:1) were used for the study. The treatment of the offspring rats was the same as that of their parents. In comparison with the control rats, the nuclei of many nerve cells were pyknosed and absent, the Nissl substance also showed various degrees of decrease, and the dendrites were elongated. The results indicate that the histopathological changes in the brain were initially due to lipid peroxidation caused by the interaction of high fluoride and low iodine. These changes in brain histopathology apparently occurred mainly during the period of embryonic development and in the early stage of brain development after birth.”

STUDY: Ge Y, et al. (2005). Comet assay of DNA damage in brain cells of adult rats exposed to high fluoride and low iodine. Fluoride 38:209-214.

“In conclusion, DNA strands in brain cell are affected adversely when rats are exposed to high fluoride, low iodine, and the interactive combination of these two factors from the age of one month to 20 months. The rate and degree of DNA damage in brain cells is higher in the High Fluoride + Low Iodine group than in either the High Fluoride or Low Iodine group.”

FLUORIDE & REDUCED IQ IN CHILDREN

COMMENTARY: The following study by Wang is the latest of a growing number of studies from China reporting an impairment in mental ability among fluoride-exposed children. For more information on these studies, see: http://www.fluoridealert.org/health/brain/

STUDY: Wang S, et al. (2005). Investigation and evaluation on intelligence and growth of children in endemic fluorosis and arsenism areas. Chinese Journal of Endemiology 24:179-182.

“This study investigated the effects of arsenism and fluorosis on the mental ability (MA) and growth of children living in areas endemic for arsenism, fluorosis , or both. The children were divided into high arsenic/fluoride group (group 1), high fluoride group (group 2), high arsenic group (group 3), and control group. Group 2 [high fluoride group] showed significantly lower MA [mental ability] than the control group ( P<0.01). MA was lower in group 1 than in the control group (P<0.05), but was almost similar between group 1 and group 2 (P>0.05). Group 3 showed the lowest MA score among the groups (P <0.01). The MA score was negatively correlated with urinary arsenic (P<0.01) and fluoride levels (P<0.05). The height of group 2 and the body weight of group 3 children were significantly lower than those of the control group ( P<0.05). The vital capacity of group 1 was significantly lower than that of control children (P<0.05). It is concluded that high exposure to arsenic, fluoride, or both has significant negative effects on the MA and growth of children.”

FLUORIDE & SKELETAL FLUOROSIS

STUDY: Bai G, et al. (2005). Radiological analysis of endemic skeletal fluorosis in Dingbian county, Shaanxi province. Chinese Journal of Endemiology 24:73-74.

“Objective: To determine radiological changes in bones and joints among patients in Dingbian County, China, where fluorosis is related to the supply of drinking water. Methods: Radiographic films of the pelvis, right forearm, and right leg were evaluated for randomly selected patients. Results: Based on the results of the radiographic films, the detection rate of skeletal fluorosis was 72.23%. Skeletal changes were seen more on the forearm and legs as compared to the pelvis. However, the radiographic diagnosis did not correspond to the clinical diagnosis. Radiographic changes were positively correlated with fluoride content in the drinking water. Thus, early diagnosis of fluorosis is difficult due to non-concordance of clinical features with radiographic changes.”

COMMENTARY: Bai’s study is interesting in that it contradicts an important bit of orthodoxy long utilized by scientists working for fluoride-polluting industries. The orthodoxy to date has been that fluoride does not pose any risks to an individual’s health prior to, and in the absence of, major changes to the skeleton. Thus, if a worker is experiencing symptoms associated with fluoride toxicity (e.g. degenerative arthritis), these symptoms are dismissed as unrelated to fluoride if x-rays of the workers’ bones do not reveal obvious fluorotic changes in the worker’s bones. (This orthodoxy has proven quite useful for industry, but quite detrimental to the health of industrial workers.)

The study by Bai has added yet further evidence of the problems with industry’s reliance on x-rays as a means of detecting early fluoride injury. As noted by Bai, the symptoms of fluorosis do not always correspond with the degree of bone changes detectable by x-ray. Thus, someone experiencing fluoride-induced arthritis may have very little obvious change to their bone structure, while another person with obvious changes to their bone structure may not always experience arthritic pain. According, therefore, to Bai, “early diagnosis of fluorosis is difficult due to non-concordance of clinical features with radiographic changes.”

For more information on the difficulty of diagnosing the early stages of skeletal fluorosis, click here.

STUDY: Sun DJ et al. (2005). Dose-response relationship between dental fluorosis and fluoride in brick tea. Abstract. Presented at the 26th International Society for Fluoride Research in Wiesbaden, Germany (September 2005). Fluoride 38(3):253.

“The dose-response relationship between fluoride in brick-tea and the prevalence of skeletal fluorosis (SF) in adults was studied to determine a safe upper limit for fluoride intake from brick-tea. In brick-tea drinking endemic fluorosis areas of the Tibetan pastoral areas of Sichuan province, cluster sampling was conducted of residents above age thirty in Amu, Jiangrong, Anqu, Longrang, and Maiwashi villages of Hongyuang County in Aba state. X-ray technology was used to diagnose SF, and the daily fluoride intake of each person from bricktea infusions was determined by a retrospective cohort study. Results: Among the 207 residents examined, the X-ray standardized prevalence rate of SF was 49.76%, which increased with age and poor health, especially among persons over age forty. Both the amount of drinking brick-tea infusions and the amount of fluoride intake from them increased with age and were higher in the SF group than that in the unaffected group. The average daily fluoride intake was 4.49±1.51 mg/person/day) in the SF group and 1.86±1.46 mg/person/day in the unaffected group. The average daily fluoride intake of subjects with different stages or grades of SF was 3.36±1.35 mg (stage I), 4.96±1.44 mg (stage II), and 6.42±1.33 mg (stage III), respectively. There was a significant (p<0.05) positive linear correlation between the logarithm of daily fluoride intake from brick-tea and the prevalence of SF in each age group. The 95% normal upper-limit for daily fluoride intake from brick-tea was 3.37 mg/person/day, but the 90% unilateral upper-limit was 2.94 mg/person/day, which reflected the SF status more truly and avoided missing and misjudging diagnosis.”

COMMENTARY: Sun’s study from China reports evidence of advanced skeletal fluorosis in communities with average daily fluoride intakes of just 6.4 mg/day. This is below the dose (10 mg/day) that the US Institute of Medicine says is safe for everyone in the population to ingest every day of their life after the age of 8. While the presence of aluminum in the brick-tea may have led to an underestimation of the total fluoride intake in this study, the authors’ dose-response analysis provides a valuable addition to the scientific literature on skeletal fluorosis. It is a study that should certainly be followed up, because, if the authors are correct, than many Americans in fluoridated and unfluoridated communities are currently ingesting a daily dose of fluoride that can cause some form of skeletal fluorosis.

FLUORIDE & the KIDNEYS

COMMENTARY: Last year, a study from China (Liu 2005) reported that children drinking water with more than 2 ppm fluoride have a higher rate of kidney disease than children drinking low fluoride water.

Included below are 4 new animal studies investigating fluoride’s effects on the kidney. While the doses used in these studies are generally higher than most humans ingest, the study by Shi (2005) found adverse effects on rat kidney at just 5 ppm fluoride in drinking water. This is quite a low concentration, particularly since rats are recognized to be more resistant to fluoride toxicity than humans. This is not, however, the first animal study to find adverse effects at low fluoride concentrations. In 1998, Varner and colleagues found damage to rat kidneys following long-term administration of just 1 ppm fluoride, while in 1999 Borke and Whitford found damage to rat kidney with just 38 parts per billion fluoride in the rats’ blood (a blood concentration routinely exceeded by humans in fluoridated areas.)

Also interesting is the finding from Birkner that the impacts of fluoride on kidney may be worsened by co-administration of caffeine. While the doses of fluoride used by Birkner were quite high relative to human exposures, their study raises important questions – particularly for habitual coffee drinkers who regularly brew their coffee (knowingly or unknowingly) with fluoridated water.

For more information on fluoride’s impact on the kidneys, click here.

STUDY: Shi Y, et al. (2005). Effects of brick tea infusion on bone, kidneys and liver morphology before and after defluoridation with serpentine. Chinese Journal of Endemiology 24: 28-30.

“Brick tea infusion containing 100 mg/litre fluorine was made according to the methods used by inhabitants living in areas (in China) with endemic fluorosis. The infusion was diluted to 5 or 50 mg/litre fluorine concentrations, followed by the de-fluoridation. Wistar rats were randomly divided into 5 groups: Group A was given tap water (control); group B and C were given brick tea with serpentine at 5.0-1.5 and 50.0-1.5 mg/litre, respectively; group D and E were given brick tea at 5 and 50 mg/litre, respectively. Fluoride contents in serum, urine and bones were determined, and the morphological changes in bones, kidneys and liver were observed under light microscopy and transmission electron microscopy. The fluoride contents in the urine and bones of fluoride treated rats were higher than that in the controls. The pathological changes in the bones, kidneys and livers were significantly more pronounced in group E [50 ppm fluoride], and followed by group D [5 ppm fluoride].”

STUDY: Xu H, et al. (2006). Effect of sodium fluoride on the expression of bcl-2 family and osteopontin in rat renal tubular cells. Biological Trace Element Research 109:55-60.

“Our earlier studies showed that the apoptosis of renal tubules can be induced by sodium fluoride (NaF). The present study was designed to estimated the effects of B-cell lymphoma/leukemia 2 (Bcl-2), Bcl-2-associated protein X (Bax), and osteopontin (OPN) on the apoptosis of renal tubular cells induced by NaF at different levels. The technique of reverse transcription-polymerase chain reaction and densitometer scanning volume density were used to evaluate the changes of Bcl-2, Bax, and OPN mRNA in tubular cells treated with different doses of NaF (0, 1, 5, 7.5, 12.5 mgF-/L) for 48 h. Compared to control, the level of Bax mRNA significantly increased at cells of the 7.5- and 12.5-mg F-/L groups and the expression of Bcl-2 mRNA obviously decreased at cells of the 5- and 7.5-mg F-/L groups. The NaF also enhanced the expression of OPN mRNA in a dose-dependent manner, but the strongest expression of OPN mRNA was observed at cells of the 7.5-mg F-/L group. The results suggested that NaF induces the apoptosis in renal tubules via activation of the Bax expression and Bcl-2 suppression; OPN probably acts as protective role against apoptosis in fluoride-treated renal cells.”

STUDY: Birkner E, et al. (2006). Influence of sodium fluoride and caffeine on the kidney function and free-radical processes in that organ in adult rats. Biological Trace Element Research 109:35-48.

“An experiment was carried out on Sprague-Dawley rats (adult males) that for 50 days were administered, in the drinking water, NaF and NaF with caffeine (doses, respectively: 4.9 mg of NaF/kg body mass/24 h and 3 mg of caffeine/kg body mass/24 h). Disturbances were noted in the functioning of kidneys, which were particularly noticeable after the administration of NaF with caffeine. Changes in the functioning of kidneys were also confirmed by such parameters as the level of creatinine, urea, protein, and calcium. Modifications of the enzymatic antioxidative system (superoxide dismutase, catalase, and glutathione peroxidase) and lipid peroxidation (malondialdehyde) were also observed. Changes in the contents of the above parameters as well as pathomorphological examinations suggest increased diuresis, resulting in dehydration of the rats examined.”

STUDY: Zhang W, et al. (2005). Intracellular ionized calcium level and oxidative stress in renal of Wistar rats after intaking of excessive fluoride. Chinese Journal of Endemiology 23: 25-27.

“The effects of excessive fluoride intake on intracellular ionized calcium level and oxidative stress in kidneys of Wistar rats were determined. The rats were fed sodium fluoride in drinking water. The intracellular ionized calcium level was measured using fura-2/AM, and glutathione peroxidase (GSH-Px), superoxide dismutase (SOD) and malondialdehyde (MDA) levels were tested using biochemical methods. Results revealed that intracellular ionized calcium level was increased in fluoride-exposed group as compared to control group. The same increase was observed between the low calcium + fluoride group and low calcium group. SOD activity was lower, whereas MDA level was higher in low calcium + fluoride group than in low calcium group. It is suggested that the higher level of intracellular ionized calcium and oxidative stress are possibly significant in fluorosis pathology. The high level of intracellular ionized calcium and oxidative stress after excessive fluoride intake, along with low calcium, indicate that calcium nutrition has close connection with fluorosis mechanism.”