A Second Look at Fluoride Exposure and Hip Fractures from Fluoride Action Network
In critiquing the York Review I spent
a considerable time reading the literature on Hip Fractures and
exposure to fluoride. I thought readers would find it helpful to have an
up-to-date list of the studies published since 1990. While the evidence
from these human epidemiological studies is mixed, when the issue is
examined in the context of the Precautionary Principle the case for not
putting fluoride
into our drinking water, with the commensurate build-up of fluoride in our bones over a lifetime, is overwhelming in my view. What do you think?
Paul Connett.
A SECOND LOOK AT FLUORIDE EXPOSURE AND HIP FRACTURES.
1. When people first hear about a possible link between water fluoridation and an increase in hip fractures among the elderly it usually doesn’t excite the same kind of reaction as the possible relationship with diseases like cancer, or damage to the central nervous system. However, any increase in hip fractures in the elderly is very serious indeed. According to Jacobsen (1992) “Hip fractures constitute a major cause of morbidity and mortality in persons aged 65 and older. An estimated 200,000 hip fractures occur in the United States each year, with an associated cost of over $7 billion. According to Phipps (1995), “As a result of osteoporosis-related hip fractures, as many as 50,000 people will die and as many as 20 per cent will be admitted for long term care in a nursing home”. To see what this could mean in terms of increased deaths from water fluoridation consider the paper by Jacobsen et al who examined over 200,000 hip fractures in men and women over 65 in the US and compared the number of fractures in fluoridated counties compared to non-fluoridated counties. They found a relative risk ratio of 1.08 for women and 1.17 for men which were both statistically significant. If we ignore all the caveats about these findings, a RR of 1.08 for women means an 8% increase in hip fractures. If we now assume that half the 200,000 hip fractures in the US for people of 65 and older, are for women (it is actually a larger fraction, as women are more prone to hip fractures after menopause) then an 8% increase represents an extra 8,000 hip fractures. If we now assume that one in four of these women will be dead in less than a year after the fracture (the national average, see Phipps, 1995) then fluoridation could contribute to 2000 extra deaths for women over 65. Thus a lot hinges on whether the findings of Jacobsen et al are valid. Clearly, this is a very important issue to resolve.
2. To date (August, 2000), since 1990, there have been 18 studies investigating the relationship between fluoride exposure via the water supply (both natural and artificial) and the incidence of hip fracture in the elderly. The lead authors of these studies are Jacobson (1990); Cooper (1990, revised in a 1991 letter to JAMA); Sowers (1991); Keller (1991, unpublished); May (1991, unpublished); Jacobson (1992); Danielson (1992); Suarez-Almazor (1993); Jacobson (1993); Cauley (1995); Jacqmin-Gadda (1995, letter to JAMA); Karagas (1996); Jacqmin-Gadda (1998); Lehmann (1998); Phipps (1999, unpublished); Li (1999, unpublished); Hellier (2000), and Hegmann ( 2000, abstract). The full references are given below.
3. Of these 18 studies, 4 are unpublished, 1 is only available as an abstract, 2 appear as letters to the Journal of the American Medical Association. Of the 18, 10 studies show an association between fluoride exposure and increased hip fracture, but 8 do not. Some studies show an association for both women and men, some for women only and some for only certain age ranges. Some studies show an increased risk for increased time of exposure, some do not. One (Li (1999, unpublished) shows a linear increase in risk with level of fluoride concentration in the water from 1 ppm up to over 4 ppm. Some authors (e.g. Jacobson and Cooper) have co-authored studies which have found an association in one study, but not in another.
4. Clearly, the issue has not been proved one way or the other. What has hindered a more definitive conclusion is the almost universal failure (Hellier is an exception) to couple the outcomes with some kind of biomarker of fluoride exposure. Instead, most authors have used the level of fluoride in the water as an indicator of exposure (i.e. dose) which, in the case of countries where fluoride is present in processed foods, beverages, pesticide residues and dental products, is not a good assumption. This underlines the incredibly incompetent failure of governments (particularly the US government) to track the build up of fluoride in the bones of the public. These levels could have been tracked as a function of fluoride levels in the water, hardness or softness of water, diet, disease status, age, sex, race etc. These bone levels would have been invaluable when probing the cause of hip fractures and other bone problems. Unfortunately, both governments and researchers are in the dark as to what our bone levels are. This is unnecessary and inexcusable.
5. So what does one do in the situation where epidemiological studies produce mixed results. One answer which is achieving growing support among a number of European governments and non-governmental organizations is to apply the Precautionary Principle. Wrapped up in this principle are four questions, which when addressed should resolve the issue of whether a population should be knowingly exposed to a toxic substance or process. These four questions are:
7. The weight of evidence.
7.1 Fluoride and the biochemistry of bone.
It is well established that about 50% of all the fluoride we ingest each day ends up in our bones and that it accumulates over a lifetime. The author of a textbook on Human Biology states: ” Perhaps because of their strength and durability, it is a popular misconception that bones are static, unchanging structures Nothing could be further from the truth. Bone is a living tissue and an extremely active one at that” (DeWitt, 1989). Fluoride has the ability to interfere with many of the enzymes in the numerous bone cells which provide different functions in bone growth and turnover. The possibilities are enormous and complicated. A brief glimpse of the complexity of this matter can be gleamed from a paper by Krook and Minor (1998). Commenting on the use of fluoride to treat osteoporosis patients, in the context of their findings in animal studies at the College of Veterinary Medicine, Cornell University, they state:
“Fluoride is a potent enzyme poison. The concept that fluoride is a specific stimulus for bone formation is preposterous…Furthermore, because fluoride injures all the cells involved in bone formation and degradation, it is not surprising that a poor quality of bone accumulates in patients treated with fluoride…It is unfortunate that many physicians who treat osteoporosis with fluoride do not realize that they are prescribing a drug that is toxic for all active bone cells”.
7.2 Bone mineral density and bone quality.
While it is true that treatment with fluoride (either short term with doses of 40 – 75 mg of fluoride, or long term with fluoridation of the water supply) can lead to an increase in bone mineral density. This turns out to be a crude index of bone health, and bone performance. Dr. Miklos Bely (1998, 2000) has performed elegant studies using a variety of microscopic and electron microscopic techniques to show the damage that fluoride does to the bone cells producing collagen and the eventual collagen formed. He concludes that while fluoride might lead to increasing the quantity of the bone, it damages its quality.
7.3 Animal studies.
Studies have shown that when rats are treated with fluoride their bones become more brittle (Wolinsky et al, 1972, Bohatyrewicz, 1999).
7.4 Human trials.
In human trials with patients with osteoporosis, it has been shown that high doses of fluoride (40 -75 mg per day) lead to more brittle bones and increased hip fracture rates (Hedlund, 1989, Riggs et , 1990).
7.5 Taking all of the above into account, as well as the mixed results from the epidemiological studies, the weight of evidence would suggest that it is highly plausible that exposure to water at 1 ppm (and the concurrent exposure to other sources of fluoride in modern life) over a whole lifetime will damage human bones and ligaments. It is also probable that this damage will at least lead to the sub-clinical symptoms of skeletal fluorosis, possibly arthritis as well as to hip fractures. This may not be true for everyone but it will probably be true for a significant minority, especially those who have a poor diet, who drink excessive quantities of water and other beverages made with fluoridated water, and those who have poor renal clearance.
8. Is the outcome of concern serious?
The outcome of increased hip fracture in the elderly is very serious. Each year some 200,000 elderly people in the US have hip fracture. The annual costs of treatment are estimated as high as 10 billion dollars. Treatment is highly traumatic for the elderly. One in four of the elderly who suffer a hip fracture are dead within one year of their operation.
9. How large is the benefit being pursued?
The reduction of dental caries ascribed to water fluoridation is not very great when compared to communities which have not fluoridated their water. Surveys in the US, Canada, Europe, Australia and New Zealand are indicating very little difference in dental decay in children from fluoridated and non-fluoridated communities ( Ziegelbecker (1981), Diesendorf (1986), Colquhoun (1987, 1994), Yiamouyiannis (1990), De Liefde (1998)). Most countries in Europe do not fluoridate their water and their children’s teeth are as good if not better than those of children in fluoridated countries.
10. Are there alternatives which achieve the benefit without triggering the same risk?
Yes there are. Some would argue that fluoride is neither necessary nor essential for healthy teeth. That a combination of a good diet, minimizing sugar consumption, and regular brushing with any kind of toothpaste or toothpaste substitute (salt, baking soda, even soap) is just as effective. Others would argue that fluoride is beneficial to achieving good teeth, especially where it is difficult to get children to limit their input of sugar and sugary foods, but that applying the fluoride in the form of fluoridated toothpaste is more effective and more appropriate, than swallowing the fluoride in drinking water. This is reinforced by leading dental researchers like Dr. Hardy Limeback , who stress that the benefits of fluoride are topical not systemic. Thus topical application of fluoride maximizes the perceived benefit while minimizing the risks of hip fracture and other possible diseases, which are caused by fluoride acting systemically. While some researchers like Dr. Susheela (who has published over 100 papers on fluoride) argue that fluoride can be absorbed through the gums from fluoridated toothpaste, I would argue that these risks are still lower than those obtained from swallowing the stuff wholesale from the water. That alternatives exist, and work, is supported by the fact that the majority of European countries do not fluoridate their drinking water and yet their childrens’ teeth are just as good, if not better, than those of fluoridated countries. Some European countries also use fluoridated salt, milk and other topical treatments as part of their strategy in fighting tooth decay
11. Thus on all these counts, an application of the Precautionary Principle would require a government to reject water fluoridation on the outcome of hip fracture alone.
12. An important aspect of the Precautionary Principle is that it builds a bridge between scientific analysis and ethical judgement. Even if only a small minority of people have their bones affected as a consequence of water fluoridation, it would raise several ethical questions. How big does this minority have to be before the ethical arguments kick in? How can one justify the protection of the teeth of one section of the community, while damaging the bones of another? Are people being given the opportunity for “informed consent” to this trade off? How can one justify even the possibility of this damage when there are known alternatives to protecting teeth as well as known ways of delivering fluoride which do not involve cumulative systemic exposure?
References.
A. The 18 studies on Hip Fracture and Fluoride Exposure since 1990.
1. Cauley, J., P. Murphy, et al. (1995). “Effects of fluoridated drinking water on bone mass and fractures: the study of osteoporotic fractures.” J Bone Min Res 10(7): 1076-86.
2. a) Cooper, C., C. Wickham, et al. (1991). “Water fluoridation and hip fracture.” JAMA 266: 513-514 (letter, a reanalysis of data presented in 1990 paper).
2. b) Cooper, C., C. Wickham, et al. (1990). “Water fluoride concentration and fracture of the proximal femur.” J Epidemiol Community Health 44: 17-19.
3. Danielson, C., J. L. Lyon, et al. (1992). “Hip fractures and fluoridation in Utah’s elderly population.” Jama 268(6): 746-748.
4. Hegmann, K.T. et al (2000) the Effects of Fluoridation on Degenerative Joint Disease (DJD) and Hip Fractures.Abstract #71, of the 33rd Annual Meeting of the Society For Epidemiological research, June 15-17, 2000. Published in a Supplement of Am. J. Epid.
5. Hillier, S., C. Copper, et al. (2000). “Fluoride in drinking water and risk of hip fracture in the UK: a case control study.” The Lancet 335: 265-269.
6. Jacobsen, S., J. Goldberg, et al. (1992). “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.
7. Jacobsen, S., J. Goldberg, et al. (1990). “Regional variation in the incidence of hip fracture: US white women aged 65 years and olders.” J Am Med Assoc 264(4): 500-2.
8. Jacobsen, S.J. et al (1993). Hip Fracture Incidence Before and After the Fluoridation of the Public Water Supply, Rochester, Minnesota. American Journal of Public Health, 83, 743-745.
9. a) Jacqmin-Gadda, H. (1995). “Fluorine concentration in drinking water and fractures in the elderly.” JAMA 273: 775-776 (letter).
9 b) Jacqmin-Gadda, H., A. Fourrier, et al. (1998). “Risk factors for fractures in the elderly.” Epidemiology 9(4): 417-423. (An elaboration of the 1995 study referred to in the JAMA letter).
10. Karagas,M.R. et al (1996). “Patterns of Fracture among the United States Elderly: Geographic and Fluoride Effects”. Ann. Epidemiol. 6 (3), 209-216.
11. Keller, C. (1991) Fluorides in drinking water. Unpublished results. Discussed in Gordon, S.L. and Corbin, S.B,(1992) Summary of Workshop on Drinking Water Fluoride Influence on Hip Fracture on Bone Health. Osteoporosis Int. 2, 109-117.
12. Kurttio, P., N. Gustavsson, et al. (1999). “Exposure to natural fluoride in well water and hip fracture: A cohort analysis in Finland.” American Journal of Epidemiology 150(8): 817-824.
13. Lehmann R. et al (1998). Drinking Water Fluoridation: Bone Mineral Density and Hip Fracture Incidence. Bone, 22, 273-278.
14. Li, Y., C. Liang, et al. (1999). “Effect of Long-Term Exposure to Fluoride in Drinking Water on Risks of Bone Fractures.” Submitted for publication. Contact details: Dr. Yiming Li, Loma Linda School of Dentistry, Loma Linda, California, Phone 1-909-558-8069, Fax 1-909-558-0328 and e-mail, Yli@sd.llu.edu
15. May, D.S. and Wilson, M.G. Hip fractures in relation to water fluoridation: an ecologic analysis. Unpublished data, discussed in Gordon, S.L. and Corbin S.B.,(1992), Summary of Workshop on Drinking Water Fluoride Inflruenbce on Hip Fracture on Bone Health. Osteoporosis Int. 2, 109-117.
16. Phipps, K. R. (1999). Community water fluoridation, bone mineral density and fractures. R01DE10814-02. HSR/96101800. USA, Oregon Health Sciences University, 611 SW Campus Dr, Portland, OR 97201, IR: (503) 494-8895,. 199309: National Institute of Dental Research (NIDR) – Grant: Noncompeting Continuation (5). To be published in the British Medical Journal.
17. Sowers, M., M. Clark, et al. (1991). “A prospective study of bone mineral content and fracture in communities with differential fluoride exposure.” American Journal of Epidemiology 133: 649-660.
18. Suarez-Almazor, M., G. Flowerdew, et al. (1993). “The fluoridation of drinking water and hip fracture hospitalization rates in two Canadian connunities.” Am J Public Health 83: 689-693.
B. OTHER REFRENCES.
Bely, M. (1998, 2000) Presentations at both the XXII and XIII world conferences of the International Society for Fluoride Research, Bellingham, Washington and Szczecin, Poland respectively.
Bohatyrrewicz, A (1999). Effects of Fluoride on Mechanical Properties of femoral Bone in Growing Rats. Fluoride, 32 (2), 47-54.
Chlebna-Sokol, D. and Czerwinski, E. (1993) Bone structure assessment on radiographs of distal radial metaphysis in children with dental fluorosis. Fluoride, 26 (1), 37-44.
Colquhoun, J. (1987).” Child Dental Health Differences in New Zealand”. Community Health Studies, XI, 85-90.
Colqhoun, J. (1994). “Is there a benefit from water fluoridation?” Fluoride, 27 (1), 13-22.
De Liefde, B. (1998). The Decline of Caries in New Zealand Over the past 40 Years. New Zealand Dental Journal, 94, 109-113
Diesendorf, M.(1986). The Mystery of Declining Tooth Decay. Nature, 322, 125-129..
DeWitt, W. Human Biology: Form, Function and Adaptation, Scott, Forseman and Company, USA , 1989.
Diesendorf, M.(1986). The Mystery of Declining Tooth Decay. Nature, 322, 125-129..
Gordon, S.L. and Corbin, S.B. (1992). Summary of Workshop on Drinking Water Fluoride Influence on Hip Fracture on Bone Health. Osteoporosis Int2, 109-117.
Hedlund, L.R. and Gallagher, J.C. (1989). Increased Incidence of Hip Fracture in Osteoporotic Women treated with Sodium Fluoride. J. Bone. Min. Res. 4 (2), 223-225.
Krook, L. and Minor, R.R. (1998) Fluoride and Alkaline Phosphatase. Fluoride, 31. 177-82.
Phipps, K. (1995). Fluoride and Bone Health. J. Pub Health Dent. 55(5), 53-56.
Riggs, B.L. et al (1990). Effect of Fluoride treatment on the Fracture Rates in Postmenopausal Women with Osteoporosis. N. Eng. J. Med., 322, 802-809.
Yiamouyiannis, J.A. (1990). Water Fluoridation and Tooth decay: Results from the 1986-87 National Survey of U.S. Schoolchildren. Fluoride, 23, 55-67.
Ziegelbecker, R. (1981). Fluoride, 14, 123-128.
into our drinking water, with the commensurate build-up of fluoride in our bones over a lifetime, is overwhelming in my view. What do you think?
Paul Connett.
A SECOND LOOK AT FLUORIDE EXPOSURE AND HIP FRACTURES.
1. When people first hear about a possible link between water fluoridation and an increase in hip fractures among the elderly it usually doesn’t excite the same kind of reaction as the possible relationship with diseases like cancer, or damage to the central nervous system. However, any increase in hip fractures in the elderly is very serious indeed. According to Jacobsen (1992) “Hip fractures constitute a major cause of morbidity and mortality in persons aged 65 and older. An estimated 200,000 hip fractures occur in the United States each year, with an associated cost of over $7 billion. According to Phipps (1995), “As a result of osteoporosis-related hip fractures, as many as 50,000 people will die and as many as 20 per cent will be admitted for long term care in a nursing home”. To see what this could mean in terms of increased deaths from water fluoridation consider the paper by Jacobsen et al who examined over 200,000 hip fractures in men and women over 65 in the US and compared the number of fractures in fluoridated counties compared to non-fluoridated counties. They found a relative risk ratio of 1.08 for women and 1.17 for men which were both statistically significant. If we ignore all the caveats about these findings, a RR of 1.08 for women means an 8% increase in hip fractures. If we now assume that half the 200,000 hip fractures in the US for people of 65 and older, are for women (it is actually a larger fraction, as women are more prone to hip fractures after menopause) then an 8% increase represents an extra 8,000 hip fractures. If we now assume that one in four of these women will be dead in less than a year after the fracture (the national average, see Phipps, 1995) then fluoridation could contribute to 2000 extra deaths for women over 65. Thus a lot hinges on whether the findings of Jacobsen et al are valid. Clearly, this is a very important issue to resolve.
2. To date (August, 2000), since 1990, there have been 18 studies investigating the relationship between fluoride exposure via the water supply (both natural and artificial) and the incidence of hip fracture in the elderly. The lead authors of these studies are Jacobson (1990); Cooper (1990, revised in a 1991 letter to JAMA); Sowers (1991); Keller (1991, unpublished); May (1991, unpublished); Jacobson (1992); Danielson (1992); Suarez-Almazor (1993); Jacobson (1993); Cauley (1995); Jacqmin-Gadda (1995, letter to JAMA); Karagas (1996); Jacqmin-Gadda (1998); Lehmann (1998); Phipps (1999, unpublished); Li (1999, unpublished); Hellier (2000), and Hegmann ( 2000, abstract). The full references are given below.
3. Of these 18 studies, 4 are unpublished, 1 is only available as an abstract, 2 appear as letters to the Journal of the American Medical Association. Of the 18, 10 studies show an association between fluoride exposure and increased hip fracture, but 8 do not. Some studies show an association for both women and men, some for women only and some for only certain age ranges. Some studies show an increased risk for increased time of exposure, some do not. One (Li (1999, unpublished) shows a linear increase in risk with level of fluoride concentration in the water from 1 ppm up to over 4 ppm. Some authors (e.g. Jacobson and Cooper) have co-authored studies which have found an association in one study, but not in another.
4. Clearly, the issue has not been proved one way or the other. What has hindered a more definitive conclusion is the almost universal failure (Hellier is an exception) to couple the outcomes with some kind of biomarker of fluoride exposure. Instead, most authors have used the level of fluoride in the water as an indicator of exposure (i.e. dose) which, in the case of countries where fluoride is present in processed foods, beverages, pesticide residues and dental products, is not a good assumption. This underlines the incredibly incompetent failure of governments (particularly the US government) to track the build up of fluoride in the bones of the public. These levels could have been tracked as a function of fluoride levels in the water, hardness or softness of water, diet, disease status, age, sex, race etc. These bone levels would have been invaluable when probing the cause of hip fractures and other bone problems. Unfortunately, both governments and researchers are in the dark as to what our bone levels are. This is unnecessary and inexcusable.
5. So what does one do in the situation where epidemiological studies produce mixed results. One answer which is achieving growing support among a number of European governments and non-governmental organizations is to apply the Precautionary Principle. Wrapped up in this principle are four questions, which when addressed should resolve the issue of whether a population should be knowingly exposed to a toxic substance or process. These four questions are:
- What is the weight of evidence from all the studies (e.g. biochemical, animal, tissue culture and epidemiological) on the debated outcome of concern?
- How serious is the outcome of concern if you proceed with the course of action?
- How large is the benefit being pursued?
- Are there satisfactory alternatives to the course of action proposed which would avoid the outcome of concern?
7. The weight of evidence.
7.1 Fluoride and the biochemistry of bone.
It is well established that about 50% of all the fluoride we ingest each day ends up in our bones and that it accumulates over a lifetime. The author of a textbook on Human Biology states: ” Perhaps because of their strength and durability, it is a popular misconception that bones are static, unchanging structures Nothing could be further from the truth. Bone is a living tissue and an extremely active one at that” (DeWitt, 1989). Fluoride has the ability to interfere with many of the enzymes in the numerous bone cells which provide different functions in bone growth and turnover. The possibilities are enormous and complicated. A brief glimpse of the complexity of this matter can be gleamed from a paper by Krook and Minor (1998). Commenting on the use of fluoride to treat osteoporosis patients, in the context of their findings in animal studies at the College of Veterinary Medicine, Cornell University, they state:
“Fluoride is a potent enzyme poison. The concept that fluoride is a specific stimulus for bone formation is preposterous…Furthermore, because fluoride injures all the cells involved in bone formation and degradation, it is not surprising that a poor quality of bone accumulates in patients treated with fluoride…It is unfortunate that many physicians who treat osteoporosis with fluoride do not realize that they are prescribing a drug that is toxic for all active bone cells”.
7.2 Bone mineral density and bone quality.
While it is true that treatment with fluoride (either short term with doses of 40 – 75 mg of fluoride, or long term with fluoridation of the water supply) can lead to an increase in bone mineral density. This turns out to be a crude index of bone health, and bone performance. Dr. Miklos Bely (1998, 2000) has performed elegant studies using a variety of microscopic and electron microscopic techniques to show the damage that fluoride does to the bone cells producing collagen and the eventual collagen formed. He concludes that while fluoride might lead to increasing the quantity of the bone, it damages its quality.
7.3 Animal studies.
Studies have shown that when rats are treated with fluoride their bones become more brittle (Wolinsky et al, 1972, Bohatyrewicz, 1999).
7.4 Human trials.
In human trials with patients with osteoporosis, it has been shown that high doses of fluoride (40 -75 mg per day) lead to more brittle bones and increased hip fracture rates (Hedlund, 1989, Riggs et , 1990).
7.5 Taking all of the above into account, as well as the mixed results from the epidemiological studies, the weight of evidence would suggest that it is highly plausible that exposure to water at 1 ppm (and the concurrent exposure to other sources of fluoride in modern life) over a whole lifetime will damage human bones and ligaments. It is also probable that this damage will at least lead to the sub-clinical symptoms of skeletal fluorosis, possibly arthritis as well as to hip fractures. This may not be true for everyone but it will probably be true for a significant minority, especially those who have a poor diet, who drink excessive quantities of water and other beverages made with fluoridated water, and those who have poor renal clearance.
8. Is the outcome of concern serious?
The outcome of increased hip fracture in the elderly is very serious. Each year some 200,000 elderly people in the US have hip fracture. The annual costs of treatment are estimated as high as 10 billion dollars. Treatment is highly traumatic for the elderly. One in four of the elderly who suffer a hip fracture are dead within one year of their operation.
9. How large is the benefit being pursued?
The reduction of dental caries ascribed to water fluoridation is not very great when compared to communities which have not fluoridated their water. Surveys in the US, Canada, Europe, Australia and New Zealand are indicating very little difference in dental decay in children from fluoridated and non-fluoridated communities ( Ziegelbecker (1981), Diesendorf (1986), Colquhoun (1987, 1994), Yiamouyiannis (1990), De Liefde (1998)). Most countries in Europe do not fluoridate their water and their children’s teeth are as good if not better than those of children in fluoridated countries.
10. Are there alternatives which achieve the benefit without triggering the same risk?
Yes there are. Some would argue that fluoride is neither necessary nor essential for healthy teeth. That a combination of a good diet, minimizing sugar consumption, and regular brushing with any kind of toothpaste or toothpaste substitute (salt, baking soda, even soap) is just as effective. Others would argue that fluoride is beneficial to achieving good teeth, especially where it is difficult to get children to limit their input of sugar and sugary foods, but that applying the fluoride in the form of fluoridated toothpaste is more effective and more appropriate, than swallowing the fluoride in drinking water. This is reinforced by leading dental researchers like Dr. Hardy Limeback , who stress that the benefits of fluoride are topical not systemic. Thus topical application of fluoride maximizes the perceived benefit while minimizing the risks of hip fracture and other possible diseases, which are caused by fluoride acting systemically. While some researchers like Dr. Susheela (who has published over 100 papers on fluoride) argue that fluoride can be absorbed through the gums from fluoridated toothpaste, I would argue that these risks are still lower than those obtained from swallowing the stuff wholesale from the water. That alternatives exist, and work, is supported by the fact that the majority of European countries do not fluoridate their drinking water and yet their childrens’ teeth are just as good, if not better, than those of fluoridated countries. Some European countries also use fluoridated salt, milk and other topical treatments as part of their strategy in fighting tooth decay
11. Thus on all these counts, an application of the Precautionary Principle would require a government to reject water fluoridation on the outcome of hip fracture alone.
12. An important aspect of the Precautionary Principle is that it builds a bridge between scientific analysis and ethical judgement. Even if only a small minority of people have their bones affected as a consequence of water fluoridation, it would raise several ethical questions. How big does this minority have to be before the ethical arguments kick in? How can one justify the protection of the teeth of one section of the community, while damaging the bones of another? Are people being given the opportunity for “informed consent” to this trade off? How can one justify even the possibility of this damage when there are known alternatives to protecting teeth as well as known ways of delivering fluoride which do not involve cumulative systemic exposure?
References.
A. The 18 studies on Hip Fracture and Fluoride Exposure since 1990.
1. Cauley, J., P. Murphy, et al. (1995). “Effects of fluoridated drinking water on bone mass and fractures: the study of osteoporotic fractures.” J Bone Min Res 10(7): 1076-86.
2. a) Cooper, C., C. Wickham, et al. (1991). “Water fluoridation and hip fracture.” JAMA 266: 513-514 (letter, a reanalysis of data presented in 1990 paper).
2. b) Cooper, C., C. Wickham, et al. (1990). “Water fluoride concentration and fracture of the proximal femur.” J Epidemiol Community Health 44: 17-19.
3. Danielson, C., J. L. Lyon, et al. (1992). “Hip fractures and fluoridation in Utah’s elderly population.” Jama 268(6): 746-748.
4. Hegmann, K.T. et al (2000) the Effects of Fluoridation on Degenerative Joint Disease (DJD) and Hip Fractures.Abstract #71, of the 33rd Annual Meeting of the Society For Epidemiological research, June 15-17, 2000. Published in a Supplement of Am. J. Epid.
5. Hillier, S., C. Copper, et al. (2000). “Fluoride in drinking water and risk of hip fracture in the UK: a case control study.” The Lancet 335: 265-269.
6. Jacobsen, S., J. Goldberg, et al. (1992). “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.
7. Jacobsen, S., J. Goldberg, et al. (1990). “Regional variation in the incidence of hip fracture: US white women aged 65 years and olders.” J Am Med Assoc 264(4): 500-2.
8. Jacobsen, S.J. et al (1993). Hip Fracture Incidence Before and After the Fluoridation of the Public Water Supply, Rochester, Minnesota. American Journal of Public Health, 83, 743-745.
9. a) Jacqmin-Gadda, H. (1995). “Fluorine concentration in drinking water and fractures in the elderly.” JAMA 273: 775-776 (letter).
9 b) Jacqmin-Gadda, H., A. Fourrier, et al. (1998). “Risk factors for fractures in the elderly.” Epidemiology 9(4): 417-423. (An elaboration of the 1995 study referred to in the JAMA letter).
10. Karagas,M.R. et al (1996). “Patterns of Fracture among the United States Elderly: Geographic and Fluoride Effects”. Ann. Epidemiol. 6 (3), 209-216.
11. Keller, C. (1991) Fluorides in drinking water. Unpublished results. Discussed in Gordon, S.L. and Corbin, S.B,(1992) Summary of Workshop on Drinking Water Fluoride Influence on Hip Fracture on Bone Health. Osteoporosis Int. 2, 109-117.
12. Kurttio, P., N. Gustavsson, et al. (1999). “Exposure to natural fluoride in well water and hip fracture: A cohort analysis in Finland.” American Journal of Epidemiology 150(8): 817-824.
13. Lehmann R. et al (1998). Drinking Water Fluoridation: Bone Mineral Density and Hip Fracture Incidence. Bone, 22, 273-278.
14. Li, Y., C. Liang, et al. (1999). “Effect of Long-Term Exposure to Fluoride in Drinking Water on Risks of Bone Fractures.” Submitted for publication. Contact details: Dr. Yiming Li, Loma Linda School of Dentistry, Loma Linda, California, Phone 1-909-558-8069, Fax 1-909-558-0328 and e-mail, Yli@sd.llu.edu
15. May, D.S. and Wilson, M.G. Hip fractures in relation to water fluoridation: an ecologic analysis. Unpublished data, discussed in Gordon, S.L. and Corbin S.B.,(1992), Summary of Workshop on Drinking Water Fluoride Inflruenbce on Hip Fracture on Bone Health. Osteoporosis Int. 2, 109-117.
16. Phipps, K. R. (1999). Community water fluoridation, bone mineral density and fractures. R01DE10814-02. HSR/96101800. USA, Oregon Health Sciences University, 611 SW Campus Dr, Portland, OR 97201, IR: (503) 494-8895,. 199309: National Institute of Dental Research (NIDR) – Grant: Noncompeting Continuation (5). To be published in the British Medical Journal.
17. Sowers, M., M. Clark, et al. (1991). “A prospective study of bone mineral content and fracture in communities with differential fluoride exposure.” American Journal of Epidemiology 133: 649-660.
18. Suarez-Almazor, M., G. Flowerdew, et al. (1993). “The fluoridation of drinking water and hip fracture hospitalization rates in two Canadian connunities.” Am J Public Health 83: 689-693.
B. OTHER REFRENCES.
Bely, M. (1998, 2000) Presentations at both the XXII and XIII world conferences of the International Society for Fluoride Research, Bellingham, Washington and Szczecin, Poland respectively.
Bohatyrrewicz, A (1999). Effects of Fluoride on Mechanical Properties of femoral Bone in Growing Rats. Fluoride, 32 (2), 47-54.
Chlebna-Sokol, D. and Czerwinski, E. (1993) Bone structure assessment on radiographs of distal radial metaphysis in children with dental fluorosis. Fluoride, 26 (1), 37-44.
Colquhoun, J. (1987).” Child Dental Health Differences in New Zealand”. Community Health Studies, XI, 85-90.
Colqhoun, J. (1994). “Is there a benefit from water fluoridation?” Fluoride, 27 (1), 13-22.
De Liefde, B. (1998). The Decline of Caries in New Zealand Over the past 40 Years. New Zealand Dental Journal, 94, 109-113
Diesendorf, M.(1986). The Mystery of Declining Tooth Decay. Nature, 322, 125-129..
DeWitt, W. Human Biology: Form, Function and Adaptation, Scott, Forseman and Company, USA , 1989.
Diesendorf, M.(1986). The Mystery of Declining Tooth Decay. Nature, 322, 125-129..
Gordon, S.L. and Corbin, S.B. (1992). Summary of Workshop on Drinking Water Fluoride Influence on Hip Fracture on Bone Health. Osteoporosis Int2, 109-117.
Hedlund, L.R. and Gallagher, J.C. (1989). Increased Incidence of Hip Fracture in Osteoporotic Women treated with Sodium Fluoride. J. Bone. Min. Res. 4 (2), 223-225.
Krook, L. and Minor, R.R. (1998) Fluoride and Alkaline Phosphatase. Fluoride, 31. 177-82.
Phipps, K. (1995). Fluoride and Bone Health. J. Pub Health Dent. 55(5), 53-56.
Riggs, B.L. et al (1990). Effect of Fluoride treatment on the Fracture Rates in Postmenopausal Women with Osteoporosis. N. Eng. J. Med., 322, 802-809.
Yiamouyiannis, J.A. (1990). Water Fluoridation and Tooth decay: Results from the 1986-87 National Survey of U.S. Schoolchildren. Fluoride, 23, 55-67.
Ziegelbecker, R. (1981). Fluoride, 14, 123-128.
Print 
PDF
No comments:
Post a Comment