Fluoridation & Hip Fracture

1993; 26(4): 274-277.

Fluoridation & Hip Fracture

by Dr. John R. Lee

Fluoride's bone effect is considered by most authorities world-wide to be toxic: bone density may increase but histomorphologic studies reveal areas of bone destruction, and fracture rates, especially of the hip, increase. The National Research Council (NRC) reviewed three US studies (1-3) and one European study (4) of osteoporosis "therapy" using sodium fluoride (NaF) in doses of 50-80 mg (20-32 mg of fluoride) daily, equivalent to 5-10 times the daily fluoride intake of persons living in fluoridated communities. They report that in all three US studies hip fracture rates increased significantly compared to controls and that, in all the studies, periarticular joint pain and gastrointestinal side effects afflicted the fluoride-treated groups. The NRC stated no conclusion from these findings. However, in an independent review of "therapeutic" fluoride treatments, Dr Avioli, Shoenberg Professor of Medicine and Director, Division of Endocrinology and Mineral Metabolism, at the Washington University School of Medicine, concluded that "sodium fluoride is accompanied by so many medical complications and side effects that it is hardly worth exploring in depth as a therapeutic mode for post-menopausal osteoporosis" (5). Not mentioned by the NRC was the Hedlund and Gallagher study (6) which likewise found a fluoride-induced increase in hip fracture.

The NRC also reviewed 10 studies comparing fracture incidence relative to fluoridation status. Seven (8,10-13,16,17) found a positive correlation (ie., increased hip fracture incidence) of fluoridation and hip fracture while three (7, 14, 15) reportedly did not. None reported any fluoride bone benefit. Two of the seven positive studies were presentations made at the Workshop on Drinking Water Fluoride Influence on Hip Fractures and Bone Health (April 10 1991, Bethesda MD) and all of the remaining five were published in major peer-reviewed journals. In spite of this array of evidence linking fluoridation to hip fracture, the NRC concluded that the three negative studies were of sufficient relevance to out-weigh the findings of the seven positive studies. Let us look at the three studies that reported no fluoride effect.

The first, by Cauley et al referenced only by an abstract in the American Journal of Epidemiology, looked at 1, 878 white women aged 65-93 years (mean age: 70.9) only 73% of whom had exposure to public drinking water, with a mean exposure time of only 6.0 years. Since bone turnover (remodelling) rate is relatively rapid before menopause and slow after menopause, fluoride's major effect on bone is most likely to occur during the years before menopause (i.e., before age 45-50), as was clearly shown in Danielson's study, Thus, none of the women in this study were exposed to fluoride during the time in their life when fluoride would be expected to affect bone. The study, therefore, is useless and should be discarded.

The second, the last of the Jacobsen studies reviewed by the NRC, and reported as a Public Health Brief in the American Journal of Public Health, suffers the same problem, i.e., few if any of the women studied were exposed to fluoridated water prior to menopause. For reason unknown, he reviewed data only through 1969, the ten years after fluoridation of Rochester MN, the site of the Mayo Clinic. Where were the data through 1979 or 1989? The Mayo Clinic is good at keeping such data. By using those, he could have observed the hip fracture incidence of women who had been premenopausal prior to being fluoridated. Even worse is the fact that the population studied (<50,000) was just too small. During the 20 years covered by the study, there were only 383 hip fractures in women and 268 in men; i.e., less than 20 per year among women and only about 1 per month among men. The annual variation in the incidence of hip fracture prior to fluoridation was over 100% and the range of standard error (95% confidence interval) was approximately 300%. If one were looking for, say a 40% fluoride-induced increase in fracture incidence, it could not have been found. The authors' own conclusions state that fluoridation in these age groups was "not associated with an immediate increase in rates of hip fractures" and that "further studies .... are clearly required before public policy decisions can be made." It has been reported that, when Jacobsen himself was asked if his study could be used to prove whether or not fluoride had a deleterious effect on fracture rates, his answer was "No". This study, too, must be discarded.

The third, a 28-year-old study by Goggin et al, looked at the hip fracture rates of women over 60 years of age for the 5 years before and after fluoridation of Elmira NY, in 1960 when the population was only 46,517 (similar to Rochester MN). Again we see that 1) the women had all passed through menopause prior to fluoridation, and 2) the number of women in the study is too small for the purpose of the study. Therefore, this study, too, is useless and must be discarded.

Interestingly, the Lancet of July 24 1993, in their section Facts, Figures, and Fallacies, carries a timely article entitled "Is the study worth doing? ". It points out the elementary statistical fact that the degree of uncertainty increases with decreasing sample size and states: "studies that are too small may fail to detect medically important effects or produce estimates too imprecise to be useful". It is apparent that NRC failed to employ the services of any competent statistician in even including these three useless studies for their consideration.

With seven studies showing a positive correlation of fluoridation with increased hip fracture incidence and not one acceptable study showing the contrary, on what basis does the NRC conclude that the fluoride MCL (maximum contaminant level) be left at 4 mg/L? They argue, without the least evidence, that there exists a "publication bias" in favor of ecologic studies showing positive results. Even if true, what does it matter? A study can either stand on its merits or it can't. They do not mention that public health reports are routinely published as a "public service" by legitimate medical journals without any independent peer review. Their second argument is that, because of un-named "limitations of ecologic analyses" and "the potential in all studies for confounding factors", the positive studies "offer only limited support for a hypothesis of a weak association between fluoridated water and hip fracture." They do admit, however, that "when results from a number of such studies converge to indicate an exposure-disease relation, confidence in collected findings is bolstered." In a remarkable feat of denial, they then conclude "there is no basis at this time to recommend that EPA lower the current MCL of fluoride of 4 mg/L."

Further, they call for additional studies that "should use information from individuals rather than population groups," stating that "it is important that individual information be collected about fluoride intake from drinking water and all other sources" plus hormone status, dietary factors, and other factors that "might influence the risk." If the NRC truly believed that, they should be calling for the throwing out of all the previous dental caries studies as well since the same argument applies.

This obvious selective reasoning does not speak well of the NRC report. Such deviousness is employed not for truth finding but for political ends and, as such, is a disservice not only to the cause of science but to the people of the US. Given the data available, it is impossible to conclude that fluoride is safe. When the NRC concludes otherwise, one must question whether they are competent to evaluate scientific studies, or whether they are guilty of a deliberate lie. If merely the data of this one chapter of the report (chapter 3) is properly analyzed, the only responsible conclusion is that 1) total daily fluoride exposure should be reduced, 2) the MCL for fluoride should be lowered, and 3) the addition of fluoride to public drinking water should be ended.

References

1. Dambacher MA, Ittner J, Ruegsegger P. Long-term fluoride therapy of postmenopausal osteoporosis. Bone 7 199-205 1986.
2. Riggs BL, Hodgson SF, O'Fallon WM et al. Effect of fluoride treatment on the fracture rate in postmenopausal women with osteoporosis. New England Journal of Medicine 322 802-809 1990.
3. Kleerekoper ME, Peterson E, Phillips E et al. Continuous sodium fluoride therapy does not reduce vertebral fracture rate in postmenopausal osteoporosis (Abstract). Journal of Bone and Mineral Research 4 (Suppl 1) S376 1989.
4. Mamelle N, Dusan R, Martin JL et al. Risk-benefit ratio of sodium fluoride treatment in primary vertebral osteoporosis. Lancet 2 361-365 1988.
5. Avioli LV. Fluoride treatment of osteoporosis. Postgraduate Medicine: special report 26-27 14 Sept 1987.
6. Hedlund LR Gallagher JC. Increased incidence of hip fracture in osteoporotic women treated with sodium fluoride. Journal of Bone and Mineral Research 4 223-225 1989.
7. Cauley JA Murphy PA, Riley T, Black D. Public health bonus of water fluoridation: Does fluoridation prevent osteoporosis and its related fractures? (Abstract) American Journal of Epidemiology 134 768 1991.
8. Sowers MFR, Clark MK, Jannausch ML, Wallace RB. A prospective study of bone mineral content and fracture in communities with differential fluoride exposure. American Journal of Epidemiology 133 649-660 1991
9. Sowers MFR, Wallace RB, Lemke JH. The relationship of bone mass and fracture history to fluoride and calcium intake: a study of three communities. American Journal of Clinical Nutrition 44 889-898 1986.
10. Keller C. Fluorides in drinking water. Paper presented at the Workshop on Drinking Water Fluoride Influence on Hip Fractures and Bone Health. Bethesda MD April 10 1991.
11. May DS, Wilson MG. Hip fractures in relation to water fluoridation. an ecologic analysis. Paper presented at the Workshop on Drinking Water Fluoride Influence on Hip Fractures and Bone Health. Bethesda MD April 10 1991.
12. Jacobsen SJ, Goldberg J, Miles TP et al. Regional variation in the incidence of hip fracture among white women aged 65 years and older. Journal of the American Medical Association 26-4 500-502 1990.
13. Jacobsen SJ, Goldberg J, Cooper C, Lockwood SA. The association between water fluoridation and hip fracture among white women and men aged 65 years and older. A national ecologic study. Annals of Epidemiology 2 617-626 1992.
14. Jacobsen SJ, O'Fallon WM, Melton III U. Hip fracture incidence before and after fluoridation of the public water supply, Rochester, Minnesota. American Journal of Public Health 83 743-745 1993.
15. Goggin JE, Haddon W, Hambly GS, HoveIand JR. Incidence of femoral fractures in postmenopausal women. Public Health Reports 80 1005-1012 1965.
16. Danielson C, Lyon JL, Egger M, Goodenough GK. Hip fractures and fluoridation in Utah's elderly population. Journal of the American Medical Association 268 746-774 1992.
17. Cooper C, Wickham CAC, Barker DJR, Jacobsen SJ. Water fluoridation and hip fracture. (Letter) Journal of the American Medical Association 266 513-514 1991.

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