The Case Against Fluoride

by Paul Connett

  It wasn’t until the Mayo Clinic doctors identified fluorosis as the cause of her pain that the woman took steps to reduce her tea intake, which led, at last, to a diminution of symptoms. According to the Mayo doctors, “Fluoride toxicity can present in an insidious manner, and clinicians may overlook its signs and symptoms. Unless recognized and the source of excessive fluoride identified and discontinued, fluoride toxicity can be both progressive and crippling. ”21

  Whyte et al. 2007

  In a third study, doctors reported a similar scenario. A forty-nine-year-old woman (without kidney disease) developed skeletal fluorosis by drinking large volumes of instant tea made with fluoridated water. As with the above cases, the woman “developed widespread musculoskeletal pains” and was misdiagnosed for years as having fibromyalgia and osteoarthritis. The authors stated:

  We surmise that habitual consumption of 3 quarts daily of some regular-strength preparations for more than 10 years, especially if made with fluoridated water, could cause clinically significant skeletal fluorosis. . . This fluoride exposure seems possible for many individuals who like instant or bottled teas. In fact, when a 36-year old coworker learned of our index case, she confided drinking 3–4 qts daily of what she described as a triple strength preparation of Nestea dissolved in unfiltered, municipal tap water over the past year. . . With increasing use of DXA [bone density scans], additional instances of skeletal fluorosis from instant tea will likely be revealed. 22

  Fluoride and Hip Fracture

  Hip fracture is a very serious issue for the elderly. About 300, 000 Americans are hospitalized for a hip fracture every year. “In the UK, the mortality following a fractured neck of femur is between 20 percent and 35 percent within one year in patients aged 82 ± 7 years. ”23 Many patients never regain an independent existence. 24, 25 Thus, if fluoridation were to increase the rates of hip fracture in the elderly, it would be serious and certainly grounds in itself to eliminate water fluoridation.

  In our view, the best way to resolve the issue of whether fluoridation increases hip fractures in the elderly is to use a “weight-of-evidence” approach, which avails itself of all the evidence that can be brought to bear on this matter, including clinical trials, animal studies. and epidemiological studies. The 2006 NRC review used this approach, and the majority of the panel concluded that bones are not protected at the current safe drinking water standard of 4 ppm. Lowering the MCLG (maximum contaminant level goal) would reduce the risk of fractures, especially for those with poor kidney function and others who are prone to accumulate fluoride in their bones. 26

  Neither the York Review27 nor the 2007 review by the NHMRC28 used a weight-of-evidence approach. Instead, both used a meta-analysis of the very limited database of epidemiological studies that examined only fracture rates with fluoride concentrations close to 1 ppm, thereby missing the significance of the trend observed by Li et al. (see “Li et al. 2001” below).

  One danger of limiting an assessment of this problem to epidemiological studies is that we are always looking at the past; by the time those studies show a definitive result, it is far too late to be of help to people who have already been exposed. The use of clinical trials and animal studies, as well as epidemiological studies, allows us a better opportunity to protect future generations— that is, before exposure has taken place. Another approach would be to apply the precautionary principle when reasonable warning signals are presented of a potential problem (see chapter 21). On fluoride’s impact on bone, we have an abundance of warning signals, which are largely being ignored by fluoridating governments.

  Clinical Trials

  High doses of fluoride (26 mg per day on average) have been used in trials to treat patients with osteoporosis in an effort to strengthen their bones and reduce fracture rates. However, the results were disappointing; while the fluoride did increase bone mineral density, the treatment frequently led to a higher number of fractures, particularly hip fractures. Sources for eleven trials that found an increased incidence of hip fracture are given in appendix 2.

  Simple arithmetic shows that the cumulative doses used in these trials (i. e. , a high dose over a short period) are exceeded by the lifetime cumulative doses (i. e. , a low dose over a long time) ingested by many people living in fluoridated communities. 29

  Animal Studies

  Many animal studies have found that fluoride decreases the strength of bone in several species. References to twenty-two studies that show weakening of animal bone by fluoride can be found in appendix 2. The authors of some of these studies (Turner et al. ) have reported thresholds for these effects ranging from 2, 500 to 4, 500 ppm in bone.

  In nearly all of sixteen fluoridated communities examined between 1941 and 1994, one or more individuals had bone fluoride levels within that range. 30

  Epidemiological Studies

  At least nineteen studies (three unpublished, including one abstract) since 1990 have examined the possible relationship of fluoride in water and hip fractures among the elderly. Eleven of these studies found an increased hip fracture rate; eight did not. Thus, to claim, as some proponents do, that there is no evidence that hip fractures are increased in fluoridated communities is inaccurate and misleading. A more accurate statement is that the evidence is mixed. An annotated list of references to all nineteen studies is given in appendix 2.

  Li et al. 2001

  Li et al. 2001 (one of the nineteen hip fracture studies) has been used by both proponents and opponents of fluoridation to support their respective cases. It is a particularly strong study, because it looked at hip fractures in six villages in China that had six different levels of fluoride in their well water, ranging from 0. 25 ppm to 7. 97 ppm. Other than this difference, the subject populations were similar and highly homogeneous and stable, sharing similar occupations, lifestyles, and diet, as well as being free of many other possible confounding variables, such as access to other sources of fluoride and use of hormone replacement therapy. The authors controlled for a number of other factors that could influence fracture frequencies including gender, smoking, and alcohol consumption. 31

  Li et al. recorded two sets of data: (1) all fractures combined and (2) hip fractures only.

  All Fractures

  When the prevalence of all fractures was plotted for the six villages, Li et al. found what they described as a U-shaped pattern: The lowest prevalence was found in village 3 (about 3 mg/day fluoride) and the highest in villages 1 (about 0. 3 mg/day) and 6 (about 14 mg/day intake), the other villages being intermediate. The statistical confidence limits shown for these data are wide, but if the U-shaped relationship is real, it suggests that intakes of fluoride of about 3 mg/day may confer some protection against fracture compared to lower and higher intakes. The water in village 3 contained 1 ppm fluoride, so some proponents of fluoridation have argued that this supports their case for artificial fluoridation at 1 ppm. That argument is fallacious, however, since it ignores the fact that, at over 3 mg/day, fracture rates increase. This is still more evident for hip fractures (see the discussion in the next section). Without the ability to control water intake and fluoride from other sources, keeping intakes at or near 3 mg/day for everyone would be impossible. There are many other sources of fluoride besides the water in fluoridating countries but no other significant sources in the rural Chinese villages studied by Li et al.

  Source: Li et al. , 2001. 32

  Figure 17. 1. Prevalence of all bone fractures (since the age of twenty years) plotted against average daily fluoride intakes in six Chinese populations; data from Li et al. , summarized in table 17. 1. 33

  Table 17. 1 summarizes Li’s data for all fractures, and in figure 17. 1 we have plotted the prevalence of all fractures in the six villages against Li’s estimated daily intake for each village in mg/day.

  Hip Fractures Only

  When the prevalence of hip fractures alone was plotted for the six villages against Li’s estimated daily intakes for each village (as tabulated in table 17. 2), no
U-shaped pattern was apparent: The prevalence was low in villages 1–3 and much higher in villages 4–6, with a possible rising trend across the whole range of fluoride intakes (see figure 17. 2). Thus, there was no evidence for a protective effect of low intakes of fluoride, but daily fluoride intakes above 3 mg/day appeared harmful.

  Thus, Li et al. ’s results show a clear, threefold increase in hip fractures in the village with the highest fluoride concentration (village 6) and suggest that the tendency for fractures may rise progressively from an intake of about 3 mg/day (1 ppm in the water) or possibly even lower.

  Returning to our discussion above about a possible benefit of protection against all fractures for villagers drinking fluoride in water at 3 mg/day, such a benefit is clearly negated by the much more pronounced and more serious problem of hip fractures increasing above 3 mg/day (or even lower). Readers should compare figures 17. 1 and 17. 2.

  With both figures 17. 1 and 17. 2 in front of us, it may astonish readers to learn that a New York State Health Department official presented this study before the village board in Corning, New York, in 2007, to support his claim that water fluoridation, which Corning was considering at the time, strengthened bones.

  Two WHO reports cite Li et al. as offering evidence that intakes of fluoride of 6 mg/day could damage bones. 34, 35 A review by the U. S. Department of Health and Human Services has estimated that fluoride exposure in fluoridated communities in the United States ranged from 1. 6 to 6. 6 mg/day, but it may be higher today and will certainly be exceeded by people who drink large amounts of water. 36

  Source: Li et al. , 2001. 37

  Figure 17. 2. Prevalence of hip fractures (since the age of twenty years) plotted against average daily fluoride intakes in six Chinese populations; data from Li et al. , summarized in table 17. 2. 38

  The finding of Li et al. is buttressed by a 1999 study from Kurttio et al. in Finland that showed an increased hip fracture rate in a subset of the elderly population exposed to fluoride above 1. 5 ppm. 39 As mentioned above, Alarcón-Herrera et al. noted an increase in bone fractures in both children and adults associated with an increase in the severity of dental fluorosis, a biomarker of exposure to fluoride before the permanent teeth have appeared. 40 These studies require confirmation, but epidemiological findings are always greatly strengthened when, as here, there appears to be a dose-related increase in the effect being studied.

  According to the 2006 NRC panel, “The combined findings of Kurttio et al. (1999), Alarcón-Herrera et al. (2001), and Li et al. (2001) lend support to gradients of exposure and fracture risk between 1 and 4 mg/L. ” 41 However, the panel members found it difficult to specify at what level increased fractures were likely to occur. Overall, the majority of the NRC panel members concluded that the current EPA MCLG of 4 ppm should be lowered: “Lowering the MCLG will prevent children from developing severe dental fluorosis and will reduce the lifelong accumulation of fluoride into bone that the majority of the committee believes is likely to put individuals at increased risk of bone fracture and possibly skeletal fluorosis, which are particular concerns for subpopulations that are prone to accumulating fluoride in their bones. ”42

  Summary

  In the sixty-year history of water fluoridation, the studies carried out on teeth in fluoridated communities vastly outnumber the studies done on bone. This reflects not the relative importance of these two systems but rather the fact that the fluoridation program has been largely driven by dental interests. It is surprising, given that 50 percent of the fluoride ingested each day accumulates in the bone, that the medical profession has not taken more interest in the matter. It does the profession little credit that bone levels of fluoride in fluoridated communities are not being monitored, an issue that we discuss further in chapter 22. Despite the paucity of study on fluoride and bone, those studies that have been carried out indicate that there is an inadequate margin of safety to protect everyone’s bones from damage over a lifetime of exposure to fluoride, especially those who have impaired kidney function.

  Bone damage can result in symptoms almost identical to the first symptoms of arthritis: aching bones and joints. Bearing in mind that more than 46 million American adults are currently diagnosed with some form of arthritis—and the numbers are expected to rise—the failure to pursue a possible connection with lifelong consumption of fluoridated water is inexplicable. A weight-of-evidence analysis of clinical trials, animal studies, and mixed epidemiological findings is highly suggestive that the accumulation of fluoride in bones from lifelong exposure to fluoride from fluoridated water and other sources will increase the risk of hip fractures in the elderly, especially those who have impaired kidney function. One important study from China (Li et al. , 2001) indicates practically no margin of safety sufficient to protect a whole population with a lifelong consumption of water at 1 ppm from hip fracture. There is enough evidence on an increase in hip fractures to show that water fluoridation should be ended.

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  Fluoride and Osteosarcoma

  Osteosarcoma is a rare but frequently fatal bone cancer found particularly in young men. With the topic of osteosarcoma and fluoride, we are talking about a possible relationship between fluoridation and deaths, few in number but nonetheless real.

  The evidence that fluoride causes osteosarcoma is not clear-cut. The studies of the relationships in both animals and humans are mixed. The issue has had a long scientific and political history.

  Observations in 1955

  While the cortical bone defects observed in the Newburgh-Kingston study were ignored as far as bone fractures were concerned (chapter 17), they did prompt discussion on another front. This is how Donald Taves described the matter in a report published by the U. S. National Academy of Sciences (NAS) in 1977:

  There was an observation in the Kingston-Newburgh (Ast et al. , 1956) study that was considered spurious and has never been followed up. There was a 13. 5% incidence of cortical defects in bone in the fluoridated community but only 7. 5% in the non-fluoridated community. With 474 and 375 children in the respective groups, the t value was 2. 85, which is statistically significant (Schlesinger, 1956). Caffey (1955) noted that the age, sex, and anatomical distribution of these bone defects are “strikingly” similar to that of osteogenic sarcoma. While progression of cortical defects to malignancies has not been observed clinically, it would be important to have direct evidence that osteogenic sarcoma rates in males under 30 have not increased with fluoridation [emphasis added]. 1

  Osteogenic sarcoma is now called osteosarcoma.

  This observation by Caffey in 1955, 2 underlined by Taves in 1977, was the beginning of a long history of concern about whether fluoridation might increase the incidence of osteosarcoma in young men. Before we look further into that history, we will first consider the “biological plausibility” of a fluoride-osteosarcoma link.

  Three key findings support the plausibility of such a link:

  1. The bone is the principal site for fluoride accumulation within the body, and the rate of accumulation is increased during periods of rapid bone development as occurs in growth spurts during childhood. Thus, the cells in the bone are exposed to some of the highest fluoride concentrations in the body.

  2. The preponderance of laboratory evidence indicates that fluoride, in sufficiently high concentrations, can cause genetic damage or genetic interference. Specifically, it can cause chromosomal damage and interfere with the enzymes involved with DNA repair, as shown in a variety of cell and tissue studies. 3–6 Recent studies have also found a correlation between fluoride exposure and chromosomal damage in humans. 7–9

  3. Fluoride is a mitogen, a substance that can stimulate cell division. It has been shown that fluoride can stimulate the proliferation of bone-forming cells (osteoblasts). 10, 11 This is important because osteosarcoma is a cancer caused by an abnormal proliferation of osteoblasts.

  According to the authors of the 2006 NRC report, “Principles of cell biology
indicate that stimuli for rapid cell division increase the risks for some of the dividing cells to become malignant, either by inducing random transforming events or by unmasking malignant cells that previously were in non-dividing states. ”12

  Fluoride and Osteosarcoma, 1975–2010

  Despite the recommendation by Taves that the rates of osteosarcoma in males under thirty be investigated in fluoridated communities, it took another thirteen years before that suggestion was followed. But before that, in 1975, further demands for research on cancer were stimulated by the work of Dr. John Yiamouyiannis, a biochemist, and Dr. Dean Burk, former head of the Cytochemistry Section of the U. S. National Cancer Institute. These two scientists stirred up a hornet’s nest when they testified before the U. S. Congress and claimed that there was a greater rate of cancer in ten fluoridated U. S. cities compared to ten non-fluoridated ones. 13 Their findings were published in Fluoride in 1977. 14

  Robert Hoover and others at the National Cancer Institute attempted to rebut these findings, claiming to have looked at the same data and found no such relationship when they adjusted for age, sex, and race. 15 Several other researchers, including Sir Richard Doll in the UK, joined in what became an intense exchange of studies, with charges and countercharges flying in both directions. The ins and outs of this debate are far too complex to resolve here.

  Meanwhile, Yiamouyiannis, Burk, and Doll have passed away. But two key players remain alive today. Dr. Robert Hoover, of the National Cancer Institute, continues to play a role in the cancer story and since 1991 has been involved in the osteosarcoma saga (see the section “Other Osteosarcoma Studies” below). John Remington Graham, a lawyer, worked very closely with Dr. Dean Burk for many years and published a recapitulation and reanalysis of his work in volume 61 of the Proceedings of the Pennsylvania Academy of Science in 1988. 16 Graham was the trial lawyer in three celebrated court cases in Pennsylvania, Illinois, and Texas from 1978 through 1984, wherein the most eminent experts in the world on both sides of this dispute testified under direct and cross-examination by seasoned trial lawyers before experienced trial judges. All three cases were settled in favor of Burk and Yiamouyiannis. With Dr. Pierre Morin, Graham has a carefully documented the legal history of this dispute for a publication of Florida State University College of Law17 as well as fleshing out the story in the book La fluoration: Autopsie d’une erreur scientifique, which has recently been republished in English. 18