Fluoride
***********************************************************************************
Why fluoride?
Some people believe fluoridation
is a profitable way for aluminum companies to dispose of a
hazard-
ous waste product. Others believe water is fluoridated to make
people docile and to inhibit thinking.
There are certainly many people who do not want to think about
it! Still others believe water is
fluoridated to protect our teeth by the same government that is
decimating us with free abortions, free
sterilizations, subsidized tobacco, subsidized sugar, lethal
swine flu shots, agent orange, radiation ex-
periments, syphilis experiments, biological experiments,
aspartame, aluminum compounds, rape seed
oil and phony wars to "halt communist expansion" while
lawyers, judges and journalists are ruthlessly
enforcing all ten planks of Marxs Communist Manifesto HERE.
This same government obviously
prefers healthy money to healthy people considering they
published a booklet titled "Keeping Our
Money Healthy where they their unlimited money would keep its
value "if there were fewer people
bidding against each other". Library of Congress Catalogue
No. 60-14368 / Revised. January 1979
Free: The Economic Consequences of Longevity by email from: hadagin@yahoo.com
How Fluoride Kills Human Cells
Researchers uncovering mechanisms behind fluoride's toxicity
Fluoride, the "Golden Child" of dental professionals around the world, seems to have a "dark side" that few outside a very specialized field of the scientific community known as "Toxicology" are aware of. As disturbing as it may be, fluoride apparently has the ability to cause DNA damage and even "cell death" in human cells.
In a new study, researchers from the National Institute for Environmental Studies in Japan note that "Even though fluoride toxicity is increasingly being considered to be important, very little information is available on the mechanism of action of fluoride."
You might think that most everything would be known about a chemical that is being added to our water and prescribed for our children, but regrettably this is not the case.
Researchers decided to investigate the mechanism by which fluoride's is able to kill cells by observing how it affects human leukemia cells. Cancerous cells are often used in research on toxicity because they are more active than normal cells.
They found that the fluoride induced a form of cell death known as "apoptosis" in a does-dependent and time dependent manner.
Now, if fluoride killing cancerous cells were the "end of the story", this would be a great breakthrough in cancer treatment and would likely save many lives. Unfortunately, things are not quite so simple.
Lead researcher Dr. C. Anuradha, in comments to the Optimal Wellness Center, explains that "fluoride in general is harmful to any type of cell. We have seen that fluoride causes cell death in other non-cancerous cells but however the mode of death has been found to be different." Instead of causing apoptosis, in normal cells fluoride seems to kill cells through a different mechanism, known as "necrosis".
Cell Death - Murder or Suicide?
Apoptosis, also known as "programmed cell death" in a process governed by genes in which the cell dies from within upon activation by some stimulating factor. It is a useful phenomenon, which occurs often as part of the normal functioning of the human body, as it gets rid of unwanted cells. The term apoptosis is derived from the Greek word that signifies "the dropping of leaves from the trees." The falling leaves are no longer needed, just as is the case with the unwanted cells, so they are gotten rid of, and recycled back into the earth.
Necrosis, on the other hand, is an externally influenced death, which occurs through some type of local injury (as loss of blood supply, corrosion, burning, or the local lesion of a disease).
A useful analogy between apoptosis and necrosis might be to compare suicide (apoptosis) to murder (necrosis).
Is it Dangerous at Much Lower Doses?
Now many readers may ask the intelligent question of - How does this affect me? Are the much lower concentrations found in fluoridated water and toothpaste a danger to my family and me?
The answer unfortunately is that nobody knows for sure. However, Dr. Anuradha states that, although the concentrations are quite low " still we expect some amount of damage even at lower concentrations, since at higher concentrations the results are quite clear that the difference is enormous and significant."
He notes that the issue of therapeutic fluoridation is the subject of much debate. Could this be the reason that Japan does not fluoridate ANY of its water supplies? This can't be said with certainty, but after all, doesn't it make sense to keep a potentially dangerous substance out of the water and not FORCE the entire population to consume it?
In the United States currently about 60% of the population drinks fluoridated water, although if the federal government has its way, that percentage will rise dramatically. This is especially true with states like California MANDATING the fluoridation of the public water supplies over a certain size.
How it Caused Cell-Death
Dr. Anuradha and colleagues found that fluoride caused apoptosis in the human leukemia cells by activating an enzyme called caspase-3, which has been identified as a key mediator of apoptosis of cells in humans and other mammals.
The authors note that "The results clearly suggest that fluoride causes cell death in HL-60 (human leukemia) cells by causing the activation of caspase-3 which in turn cleaves PARP leading to DNA damage and ultimately cell death."
What Type of Fluoride?
Except for readers with strong scientific backgrounds, most people don't realize that there is really no such thing as plain "fluoride". When it said that "fluoride" is added to the water, in reality it is a fluoride-compound such as sodium fluoride (NaF), which is the form used in these toxicity experiments.
While this may be the most well known and well-studied of all the fluoride compounds, it is actually very rarely used for water fluoridation. In over 90% of the fluoridated water in the US, the chemicals used are one of the silicofluorides (either fluosilicic acid or sodium silicofluoride).
However, these chemicals have been shown to act much differently from the much simpler sodium fluoride. In one study, it was shown that these chemicals enhance the cellular uptake of lead (http://www.fluoride-journal.com/98-31-3/313-s25.htm).
Being that there is evidence that silicofluorides may be even more toxic than NaF, it is quite possible that the DNA damage and cell-killing ability might be even greater in the type of fluoride used in the water supplies.
What Can I Do About it?
Whether you believe that water fluoridation is a vast conspiracy or simply that it is a possibility that fluoride is a dangerous substance that you would just rather avoid, the question remains the same - what to do about it?
The best advice would be to go to our Fluoride Links Page (http://mercola.com/article/links/fluoride_links.htm) and get involved.
Related Articles
Community
Dent Oral Epidemiol 2000 Aug;28(4):281-8 Caries in the primary dentition, after discontinuation of water fluoridation, among children receiving comprehensive dental care. Seppa L, Karkkainen S,
Hausen H The city of Kuopio in central Finland had fluoridated piped water for 33 years, beginning in 1959. Due to strong opposition by various civic groups, water fluoridation was stopped at the end of 1992. There is little information on the consequences of stopping fluoridation in a community with comprehensive dental care for all children and adolescents, who are frequently exposed to different fluoride measures both at home and in the dental office. OBJECTIVES: The aim of this repeated cross-sectional survey was to examine how discontinuation of water fluoridation in Kuopio affected caries in the primary dentition. Changes in the mean dmfs values between 1992 and 1995 in Kuopio were compared to those in Jyvaskyla, a low-fluoride community that has repeatedly been used as the reference area for Kuopio. METHODS: In 1992 and 1995, independent random samples of all children aged 3, 6 and 9 years were drawn in Kuopio and Jyvaskyla. The total number of subjects examined was 421 in 1992 and 894 in 1995. Calibrated dentists registered caries clinically and radiographically. RESULTS: In all age groups both in 1992 and 1995, the point estimates for mean dmfs values were lower in the non-fluoridated town. In both towns, the observed mean dmfs values were smaller in 1995 than in 1992. CONCLUSION: Despite discontinuation of water fluoridation, no increase of caries frequency in primary teeth was observed in Kuopio within a three-year period. Of further interest: "Even when very large sample sizes are used to obtain statistically significant results, the benefit of water fluoridation is not a clinically relevant one (the number of tooth surfaces saved from dental decay per person is less than one half). Recent studies show that halting fluoridation will either result in only a marginal increase in dental decay which cannot be detected or no increase in dental decay at all." -- Dr. Hardy Limeback, Head, Preventive Dentistry, University of Toronto & President, Canadian Association for Dental Research, April 2000 |
The Mystery of Declining Tooth Decay
Nature
July 10 1986; Vol. 322
The Mystery of Declining Tooth Decay
by Mark Diesendorf
Large temporal reductions in tooth decay, which cannot be attributed to fluoridation, have been observed in both unfluoridated and fluoridated areas of at least eight developed countries over the past thirty years. It is now time for a scientific re-examination of the alleged enormous benefits of fluoridation.
Fluoridation consists of raising the concentration of the fluoride ion F- in water supplies to about 1 part per million (p.p.m.) with the aim of reducing dental caries (tooth decay) in children. In fluoridated areas, there are now many longitudinal (temporal) studies which record large reductions in the incidence of caries (1). The results of these and of fixed time surveys have led to the 'fluoridation hypothesis', namely that the principal cause of these reductions is fluoridation.
Until the early 1980s, there had been comparatively few longitudinal studies of caries in unfluoridated communities. Only a small minority of the studies in fluoridated areas had regularly examined control populations, and there seemed to be little motivation to study other unfluoridated communities. But during the period 1979-1981, especially in western Europe where there is little fluoridation, a number of dental examinations were made and compared with surveys carried out a decade or so before. It soon became clear that large reductions in caries had been occurring in unfluoridated areas (see below). The magnitudes of these reductions are generally comparable with those observed in fluoridated areas over similar periods of time.
In this article, these reductions are reviewed and attention is also drawn to a second category is observed in children described by proponents of fluoridation as having been 'optimally exposed', that is, children who have received water fluoridated at about 1 p.p.m. from birth. The observation is that caries is declining with time in 'optimally exposed' children of a given age. In some cases, the magnitudes of these reductions are much greater in percentage terms than the earlier reductions in the same area which had been attributed to fluoridation.
The problem of explaining the two categories of reduction goes well beyond the field of dentistry: contributions from nutritionists, immunologists, bacteriologists, epidemiologists and mathematical statisticians, amongst others, may be required.
Caries in unfluoridated areas
Table 1 lists over 20 studies which report substantial temporal reductions in caries in children's permanent teeth in unfluoridated areas of the developed world. In many of these cases, the magnitudes of these reductions are comparable with those observed in fluoridated areas and attributed to fluoridation.
Table 1: Studies reporting large reductions in dental caries in unfluoridated areas |
|||
Location | Years Surveyed | References | |
Australia | Brisbane | 1954, '77 | 2,3 |
Sydney | 1961, '63, '67 | 4 | |
Denmark | Various towns | 1972, '79 | 53 |
Holland | The Hague | 1969, '72, '75, '78 | 38 |
Various towns | 1965, '80 | 11 | |
New Zealand | Auckland (parts) | 1966, '74, '81 | 12 |
Norway | Various towns | 1970, '80 | 54 |
Sweden | Various towns | 1973, '78, '81 | 39 |
North Sweden | 1967, '77 | 55 | |
United Kingdom | Bristol | 1970, '79 | 56 |
Bristol | 1973, '79 | 56 | |
Devon | 1971, '81 | 37 | |
Gloucestershire | Annually from 1964 | 37* | |
Isle of Wight | 1971, '80 | 57 | |
North-West England | 1969, '80 | 58 | |
Scotland | 1970, '80 | 59 | |
Shropshire | 1970, '80 | 10 | |
Somerset | 1975-79 annually | 60 | |
Somerset | 1963-79 | 61 | |
United States | Dedham, Mass. | 1958, '74 | 40 |
Norwood, Mass. | 1958, '72, '78 | 40 | |
Massachusetts: sample of schools | 1951, '81 | 41 | |
Ohio | 1972, '78 | 62 | |
* Unpublished Communication from J. Tee (1980), Area Dental Officer, Gloucestershire, to R. Anderson et al. 37 |
Several of these studies give clues as to factors which are unlikely to be the main causes of the reductions. A comparison of the 1954 and 1977 dental health surveys in Brisbane (2,3) indicates to a reduction of about 50% in caries, as measured by the number of decayed, missing and filled permanent teeth (DMFT) per child and averaged over the age groups, in the 23-year period. The 1977 survey distinguished between children who took fluoride tablets regularly, irregularly or not at all. Although there were differences in caries incidences between the three categories (which could reflect factors unrelated to fluoride levels), even the "no tablet" group had on average 40% less caries experience than that recorded in 1954 So fluoride tablets were not the principal cause of the reductions observed in Brisbane.
The first Sydney study (4) showed that children with "naturally sound" teeth increased from 3.8% in 1961 to 20.2% in 1967 and 28% in 1972. The paper, which was titled enthusiastically "The Dental Health Revolution", was originally used widely to promote fluoridation in Australia. The authors stated that: "Almost certainly, the availability of fluoride both in tablet form and delivered through town water supplies has been the predominant factor...These very large reductions represent a modern triumph of preventive health care" (4). Yet the major proportion of the reported improvement had already occurred before Sydney was fluoridated in 1968. Moreover, no evidence was presented that fluoride tablets were widely used in the 1960s. Fluoride toothpaste was only introduced into Australia in 1967 (3). Although the index is unsuitable for more detailed studies which distinguish decayed, missing and filled teeth, the populations examined were very large (over 9,000 children at each examination) and the results clear-cut.
A second Sydney study (5) used the DMFT index, but was irrelevant for establishing any link with fluoridation, since it reported only on examinations in 1963 and 1982, but not around 1968 when Sydney was fluoridated. As in several other fluoridation studies, the key data were either not collected or not reported (6). Although the two Sydney papers have an author in common (James S. Lawson, a senior officer of the New South Wales Health Commission), the second paper does not even cite the first. This suggests that, once it became clear that the first Sydney study contained evidence unfavorable to fluoridation, it was a source of embarrassment to some fluoridation proponents who are apparently trying to denigrate it.
However, an independent confirmation of the large reductions in caries before fluoridation reported in the first Sydney study (4) is readily obtained by comparing the results of two surveys (7,8) separated by 20 years by Barnard. These surveys showed that the mean DMFT index ('I' denotes a permanent tooth which cannot be restored) for school children aged 13 and 14 declined from 11.0 in 1954-55 to 6.0 in 1972. The four years from 1968, when fluoridation commenced in Sydney, to 1972, would not have contributed significantly to the decline in caries prevalence in this age group (9).
The authors of one of the British studies (10) cited in Table 1 point out that sales of fluoride toothpaste in the United Kingdom were less than 5% of total sales in 1970, but rose to more than 95% of sales in 1977. They quote unpublished annual data from unfluoridated parts of Gloucestershire, collected from 1964 onwards, which show substantial improvements in children's teeth before the use of fluoride toothpaste became significant.
Many of the studies in the Netherlands, reviewed by Kalsbeek (11), were carried out to evaluate the effectiveness of the school dental health programme. Temporal reductions in DMFT of about 50% occurred between 1970 and 1980, whether or not the children had taken part in the dental health education program. Kalsbeek also reviewed the use of fluoride tablets and toothpaste and concluded from the data that "factors other than the effects of different fluoride programmes must play a role."
The study in the partly fluoridated city of Auckland, New Zealand (12), examined the influence of social class (which reflects environmental and lifestyle factors, such as diet) as well as fluoridation on dental health as measured by the levels of dental treatment received by children. The paper showed that treatment levels have continued to decline in both fluoridated and unfluoridated parts of the city and that these reductions are related strongly to social class, there being less caries in the "above average social rank" group than in other children. Thus the main ethical argument for fluoridation, that it should assist the disadvantaged, is not borne out by this study.
Fluoridation's benefits
On 15 December 1980, the Dental Health Education and Research Foundation, one of the main fluoridation promotion bodies in New South Wales (NSW), issued a press release entitled, "Fluoridation dramatically cuts tooth decay in Tamworth" (13). This document, which highlighted results of a study conducted by the Department of Preventive Dentistry, Sydney University, and the Health Commission of NSW, stated in part:
Tamworth's water supply was fluoridated in 1963, and the last survey in the area was conducted in August 1979. It shows decay reductions ranging from 71% in 15-year-olds to 95% in 6-year-olds...All those surveyed were continuous residents using town water. |
The "95%" reduction actually corresponded to a reduction in DMFT from 1.3 in 1963 to 0.1 in 1979 (14), which is 92%. The press release implied incorrectly that all this reduction was due to fluoridation. However, it has been claimed that since the commencement of fluoridation that the maximum possible benefits from fluoridation are obtained in children who have drunk fluoridated water from birth. Six-year-olds would have done this by 1969, when, according to the published data (15), they had a DMFT index of 0.6. The further reduction in caries in optimally exposed 6-year-olds, observed in years following 1969, cannot be due to fluoridation.
Thus, one can say that at best fluoridation could have approximately halved the DMFT rate in 6-year-olds between 1963 and 1969. (Since there was no control population, one could also say that at worst fluoridation might have had no effect in that period.) But from 1969 to 1979, caries in 6-year-olds was reduced a further 83%, by some other factor(s) than fluoridation.
Figure 1 shows that the unknown factors caused in children of each age from 6 years to 9 years similar large reductions in caries. Unfortunately, there are no published data for Tamworth beyond 1979 or in the years between 1972 and 1979, and so it cannot be confirmed whether the large reductions observed (14,15) from 1972 to 1979 in children aged 10 to 15 were also due to these unknown factors.
A similar reduction beyond the maximum possible for fluoridation is observed for children of each age from 6 to 9 in the published data from Canberra (16), which cover the period from 1964, the stated year of fluoridation, to 1974. In particular, DMFT rates declined by 50% in 6-year-olds from 1970 to 1974 and by 54% in 7-year-olds from 1971 to 1974. These reductions in optimally exposed children cannot be due to fluoridation. Published post-1974 data are needed to check on further reductions in optimally exposed children aged over 9 years.
From 1977 onwards, data have been systematically collected from the school dental services in each Australian state and territory (9,17). Table 2 shows the degree of fluoridation in each of these states/territories in 1977 and 1983 and also the dates of fluoridation of the capital cities of these regions. Each of these cities dominates the population of the state or territory in which it lies. The evidence presented in Fig. 2 and Table 2 suggests that states and territories which had been extensively fluoridated for at least 9 years before 1977 (Tasmania, Western Australia and New South Wales) had qualitatively similar large reductions in caries from 1977 to 1983 as a state which was only extensively fluoridated in 1977 (Victoria) and a state which had a small and declining fraction of fluoridation (Queensland). Although the results of the school dental health survey are recorded by age and state, the data have only been published (9,17,18) so far for ages 6-13 averaged in each state, or for each age for the whole of Australia. There is evidence that the use of fluoride toothpaste in Australia reached a high plateau around 1978, so these observed reductions in caries can be due neither to fluoride toothpaste (9) nor to fluoridated water.
It is to be hoped that similar data on caries reductions in "optimally exposed" children will be sought in other fluoridated countries. In a region of Gloucestershire, United Kingdom where the main water supply was naturally fluoridated with 0.9 p.p.m. fluoride until 1972, reductions in caries of 51% were observed in 12-year old children between 1964 and 1979 (19). Factors other than fluoridated water must have caused these reductions. After 1972, the main water supply was drawn from a bore with less than 0.2 p.p.m. fluoride, so a recent survey of caries there would be of great interest.
Benefits overestimated?
In some fluoridated areas (for example Tamworth, Australia), temporal reductions in caries have been wrongly credited to fluoridation. The magnitude of these reductions is similar in both fluoridated and unfluoridated areas, and is also generally comparable with that traditionally attributed to fluoridation. Can it be concluded that communities which prefer not to fluoridate, either because of concern about potential health hazards (20-25) or for ethical reasons (for example compulsory medication; medication with an uncontrolled dose), do not necessarily face higher levels of tooth decay than fluoridated communities? In other words, is it reasonable to ask whether it could be generally true that a major part of the benefits currently attributed to fluoridation is really due to other causes?
Such a hypothesis would seem to be possible in principle because it is well known that fluoridation is neither 'necessary' nor 'sufficient' (the words between inverted commas being used in the formal logic sense) for sound teeth; that is, some children can have sound teeth without fluoridation, and some children can have very decayed teeth even though they consume fluoridated water (25).
To confirm or refute the hypothesis, it is necessary (but not 'sufficient') to examine the absolute values of caries prevalence in fluoridated and unfluoridated areas. If it is true that the absolute values of caries prevalence in some unfluoridated areas are comparable with those in some unfluoridated areas of the same country, then the hypothesis is supported (but not proven), and there would be a strong case for the scientific re-examination of the epidemiological studies which appear to demonstrate large benefits from fluoridation.
The earliest set of studies comparing caries in fluoridated and unfluoridated areas were time-independent surveys of caries prevalence in areas with 'high' natural levels of fluoride in water supplies, conducted by H.T. Dean and others in the United States (26). The surveys purported to show that there is an "inverse relationship" between caries and fluoride concentration. From the viewpoint of modern epidemiology, these early studies were rather primitive. They could be criticized for the virtual absence of quantitative, statistical methods, their nonrandom method of selecting data and the high sensitivity of the results to the way in which the study populations were grouped (25).
Results running counter to the alleged inverse relationship have been reported from time-independent surveys in naturally fluoridated locations in India (27), Sweden (28), Japan (29), the United States (30) and New Zealand (31,63). The Japanese survey (29) found a minimum in caries prevalence in communities with water F-concentrations in the range 0.3-0.4 p.p.m.; above and below this range, caries prevalence increased rapidly.
These surveys (27-31) also selected their study regions nonrandomly. But recently Ziegelbecker (32) attempted to make a selection close to a random sample by considering 'all' available published data on caries prevalence in naturally fluoridated areas. His large data set, which includes Dean's as a sub-set, comprises 48,000 children aged 12-14 years drawn from 136 community water supplies in seven countries. He found essentially no correlation between caries and log of fluoride concentration. The surveys (27-32) are generally omitted from lists (1) of studies on the role of fluoridation in caries prevention.
Further evidence can be drawn from Fig. 2. In 1983, the absolute value of caries prevalence in the Australian state of Queensland (which is only 5% fluoridated) was approximately equal to that in the states of Western Australia (83% fluoridated) and South Australia (70% fluoridated).
The classical British fluoridation trials at Watford and Gwalchmai were longitudinal controlled studies. In this regard they were better designed than the majority of other studies which have been conducted around the world. However, as in the case of almost all other surveys, the examinations were not 'blind.' The review of the British trials by the UK Department of Health after 11 years of fluoridation showed that children in fluoridated towns had approximately one less DMFT (that is, essentially one less cavity) than children of the same age in unfluoridated towns (see Fig. 3). The rate of increase in caries with age was the same in both populations (33).
Thus there a number of counter-examples to the widely-held belief that "All studies show that communities where water contains about 1 p.p.m. fluoride have about 50% lower caries prevalence than communities where water has much less than 1 p.p.m. fluoride".
At this point the empirical data presented here may be summarized as follows. In the developed world:
(1) there have been large temporal reductions in caries in unfluoridated areas of at least eight countries;
(2) there have been large temporal reductions in several fluoridated areas which cannot be attributed to fluoridation;
(3) the absolute values of caries prevalence in several fluoridated areas are comparable with those in several unfluoridated regions of the same country.
Hence there is a case for scientific re-examination of the experimental design and statistical analysis of those studies which appear to prove or "demonstrate" that fluoridation causes large reductions in caries. Indeed the few re-examinations which have already been done confirm that there are grounds for concern.
The original justification for fluoridation in the United States, Britain, Canada, Australia, New Zealand and several other English-speaking countries was based almost entirely on the North American studies, which were of two kinds. The limitations of the first set, the time-independent surveys conducted in naturally fluoridated areas of the United States (26), have been referred to above.
The second set of North American studies consists of five longitudinal studies -- carried out at Newburgh, Grand Rapids, Evanston and Brantford (two studies) -- which commenced in the mid 1940s. Only three of them had controls for the full period of the study. These studies were criticized rigorously in a detailed monograph by Sutton (34), on the grounds of inadequate experimental design (for example, no 'blind' examinations and inadequate baseline measurement), poor or negligible statistical analysis and, in particular, failure to take account of large variations in caries prevalence observed in the control towns. The second edition of Sutton's monograph contains reprints of replies by authors of three of the North American studies and another author, together with Sutton's comments on these replies. It is difficult to avoid the conclusion that Sutton's critique still stands. Indeed, this was even the view of the pro-fluoridation Tasmanian Royal Commission (35). Yet, in major, recent reviews of fluoridation, such as that by the British Royal College of Physicians (36), these North American studies are still referred to as providing the foundations for fluoridation, and Sutton's work (34) is not cited.
An examination has just been completed of the experimental design of all of eight published fluoridation studies conducted in Australia. One (Tasmania) is a time-independent survey. Four (Townsville, Perth, Kalgoorlie and the second Sydney study) are longitudinal studies with only two examinations of the test group and either no control or only a single examination of a comparison group. The remaining three studies (Tamworth, Canberra and the first Sydney study) have several examinations of the test group, but no comparison group at all. Thus there has not been a single controlled longitudinal study in Australia. (M.D., to be published). Moreover, it has been shown above that three of the Australian studies (the first Sydney (4), Tamworth (14,15) and Canberra (16)) inadvertently provide evidence that some other factor(s) than fluoridation is/are playing an important role in the decline of caries prevalence.
Hence the hypothesis that fluoridation has very large benefits requires re-examination by epidemiologists, mathematical statisticians and others outside of the dental profession. The danger of failing to perform scientific research on the mechanisms underlying the large reductions in caries discussed in this paper is that the strong emphasis on fluoridation and fluorides may be distracting attention away from the real major factors. These factors could actually be driving a cyclical variation of caries with time (37). It is possible that the condition of children's teeth could return to the poor state observed in the 1950s, even in the presence of a wide battery of F-treatments.
Causes of caries reductions
Many of the authors who reported the reductions in unfluoridated areas acknowledged that the explanation has not yet been determined scientifically (11, 37-41). It is after all much easier to perform a study which measures temporal changes in the prevalence of a multifactorial disease than to identify the causes of such changes.
Nevertheless, the authors of some of these studies have speculated that important causes of the reductions which they observe might be topical fluorides (38,53) (such as in toothpastes, rinses and gels), fluoride tablets (4, 38), school dental health programmes (9), a lower frequency of sugar intake (39), the widespread use of antibiotics which may be suppressing Streptococcus mutans bacteria in the mouth (41), the increase in total fluoride intake from the environment (9, 42), or a cyclical variation in time resulting from as yet unknown causes (37).
The present overview has revealed that several of the studies contain evidence against some of these proposed factors. We have seen that the Brisbane study (3) and Dutch review (11) suggest that fluoride tablets may not be important; the Sydney study (4), one of the British studies (10) and the Dutch review (110 each provides evidence against fluoride toothpaste; and the Dutch review (11) found no benefit in their school dental health education programmes.
Although there is evidence that fluoride toothpaste cannot be an important mechanism of caries reduction in some of the studies reported here, it must be stated that, unlike the case of fluoridation, there are also a few well-designed randomised controlled trials which demonstrate substantial reductions in caries from fluoride toothpaste (43). Hence, the hypothesis can be made that topical fluorides sometimes improve children's teeth, although they are not necessary. So topical fluorides may comprise one of several factors contributing to the solution of the scientific problem of explaining the reduction in tooth decay.
Leverett (42) has speculated that the caries reductions in his smaller set of unfluoridated locations may be due to "an increase in fluoride in the food chain, especially from the use of fluoridated water in food processing, increased use of infant formulas with measurable fluoride content, and even unintentional ingestion of fluoride dentrifices." This hypothesis cannot explain the reductions in prefluoridation Sydney (4), or those in unfluoridated parts of Gloucestshire which started in the late 19602 (10). The ingestion of fluoride toothpastes (and gels) by young children is well documented and could account for an intake of about 0.5 mg F- per day in the very young (44). But the food processing pathway is unlikely to be significant in western Europe where there is hardly any fluoridation, and infant formulas which are made up with unfluoridated water will give only small contributions. Thus it appears that Leverett's hypothesis may at best be relevant to a minority of the studies listed in Table 1.
Here, the working hypothesis is presented that fluoridation and other systemic uses of fluoride, such as fluoride tablets, have at best a minor effect in reducing caries; that the main causes of the observed reductions in caries are changes in dietary patterns, possible changes in the immune status of the populations and, topical fluorides. Indeed, a promising explanation is that the apparent benefit from fluorides is derived from their topical action. Then, since fluoridated water has a fluoride ion concentration 10 -3 times that of fluoride toothpaste, its action in reducing is likely to be much weaker.
It is known that immunity plays a role in the development of caries, as it does with other diseases. Research is currently in progress to try to develop a vaccine against caries (45-47). None of the data presented in the present paper provides evidence against immunity as a factor.
Dentists often argue against changes in dietary patterns as a major factor, on the grounds that sugar consumption has remained approximately constant in most developed countries over the past few decades. However, this is a simplistic argument. First, crude industry figures on total sales of sugar in developed countries contain no information on the distribution of sugar consumption with age and time of day. The form of sugar ingested -- for example in canned food, soft drinks or processed cereals -- may also be important. Second, tooth decay is increasing together with increases in sugar and other fermentable carbohydrates in the diet in several developing countries (48,49). This was also the case with Australian aborigines, even when their water supplies consisted of bores containing fluoride at close to the "optimal" concentration for the local climate (50,51). Third, there is more to diet than sugar. For instance, there is some evidence, even conceded occasionally by pro-fluoride bodies (52), that certain foods which do not contain fluorides (for example wholegrain cereals, nuts and dairy products) may protect against tooth decay. So the whole question of the relationship between total diet and tooth decay needs much greater input from nutritionists and dietitians.
Perhaps the real mystery of declining tooth decay is why so much effort has gone into poor quality research on fluoridation, instead of on the more fundamental questions of diet and immunity.
The main body of this research was performed while the author was a principle research scientist in the CSIRO Division of Mathematics ad Statistics, Canberra.
Mark Diesendorf is at the Human Sciences Program, Australian National University, GPO Box 4, Canberra ACT 2601, Australia
References:
1. Murray, J.J. & Rugg-Gunn, A.J. Fluorides in Caries Prevention 2nd Edn (Wright, Bristol, 1982).
2. Kruger, B.J. Aust. J. Dent. 59, 162-166 (1955).
3. McEniery, T.M. & Davies, G.N. Community Dent. oral Epidem. 7, 42-50 (1979).
4. Lawson, J.S., Brown, J.H. & Oliver, T.I. Med. J. Aust. 1, 124-125 (1978).
5. Burton, V.J., Rob, M.I., Craig, G.C. & Lawson, J.S. Med J. Aust 140, 405-407 (1984).
6. Sutton, P.R.N. Med J. Aust. 141, 394-395 (1984).
7. Barnard, P.D. NHMRC Spec. Rep. Ser. 8, 30-43 (National Health & Medical Research Council, Canberra, 1956).
8. Barnard, P.D., Clements, F.W. Int. dent. J. 26, 320-326.
9. Carr, L.M. Aust. dent. J. 28, 269-276 (1983).
10. Anderson, R.J., Bradnock, G. & James, P.M.C. Br. dent. J. 150, 278-281 (1981).
11. Kalsbeek, H.J. J. dent. Res. 61 (Special Issue), 1321-1326 (1982).
12. Colquhoun, J. Community Dent. Oral Epidemiol. 13, 37-41 (1985).
13. Dental Health Education & Research Foundation, News Release, Sydney, 15 December 1980.
14. Barnard, P.D. Dent. Outlook 6(4), 46-47 (1980).
15. Martin, N.D. & Barnard, P.D. Dent. Outlook no. 23, 6-7 (May, 1970); no. 33, 2-3 (May, 1972); no. 41, 6-7 (December, 1973).
16. Carr, L.M. Aust. dent. J. 21, 440-444, (1976).
17. Australia, Director-General of Health, Annual Report 1983-84, Table 69 (1984); Annual Report 1981-82, Table 66 (1982). Australian Government Publishing Service, Canberra.
18. Carr, L.M. Aust. dent. J. 27, 169-175 (1982).
19. Anderson, R.J. Br. dent. J. 150, 354-355 (1981).
20. Rose, D. & Marier, J.R. Environmental Fluoride, 1977 (National Research Council of Canada, Ottawa, 1977).
21. Waldbott, G.L., Burghstahler, A.W. & McKinney, H.L. Fluoridation: the Great Dilemma (Coronado, Lawrence, Kansas, 1978).
22. Tsutsui, T. Ide, K. & Maizumi, H. Mutat. Res. 140, 43-48 (1984).
23. Tsutsui, T., Suzuki, N., Ohmori, M. & Maizumi, H., Mutat. Res. 139, 193-198 (1984).
24. Tsutsui, T., Suzuki, N., Ohmori, M. Cancer Res. 44, 938-941 (1984).
25. Diesendorf, M. Commun. Hlth Stud. 4, 224-230 (1980).
26. McClure, F.J. (ed.) Fluoride Drinking Waters (US Department of Health, Education & Welfare, Public Health Service, Bethesda, Maryland, 1964).
27. Amrit, T. & Joshi, J.L. Conference Int. Soc. Fluoride Res., New Delhi, November, Abstr. 15 (1983).
28. Forsman, B., Commun. dent. Oral Epidem. 2, 132-148 (1974).
29. Imai, Y., Jap. J. Dent. Health 22, 144-196 (1972).
30. Zimmerman, E.R., Leone, N.C. & Arnold, F.A. J. Am. med. Ass. 50, 272-277 (1955).
31. Hewat, R.E.T. New Zealand dent. J. 45, 157-167 (1949).
32. Ziegelbecker, R. Fluoride 14, 123-128 (1981).
33. UK Dept of Health, Report No. 122, HMSO, London (1969).
34. Sutton, P.R.N. Fluoridation: Errors and Omissions in Experimental Trials 2nd edn (Melbourne University Press, Melbourne, 1960).
35. Report of the Royal Commission into Fluoridation of Public Water Supplies (Government Printer, Hobart, Tasmania, 1968).
36. Royal College of Physicians, Fluoride, Teeth and Health (Pitman Medical, London, 1976).
37. Anderson, R.J., Bradnock, G., Beal, J.F. & James, P.M.C. J. dent. Res. 61 (Special Issue), 1311-1316 (1982).
38. Truin, G.J., Plasschaert, A.J.M., Konig, K.G. & Vogels, A.L.M. Commun. Dent. oral Epidem. 9, 55-60 (1981).
39. Koch, G. J. dent. Res. 61 (Special Issue), 1340-1345 (1982).
40. Glass, R.L. Caries Res. 15, 445-450 (1981).
41. DePaola, P.F., Soparkar, P.M., Tavares, M., Allukian Jr, M. & Peterson, H., J. dent Res. 61 (Special Issue), 1356-1360 (1982).
42. Leverett, D.H. Science 217, 26-30 (`1982).
43. James, P.M.C., Anderson, R.J., Beal, J.F.& Bradnock, G. Commun. Dent. oral Epidem. 5, 67-72 (1977).
44. Ekstrand, J. & Ehrnebo, M. Caries Res. 14, 96-102 (1980); Ekstrand, J. & Koch, G., J. Dent. Res. 59, 1067 (1980).
45. Lehner, T. Russell, M.W. Caldwell, J. Lancet i, 995-997 (1980).
46. McGhee, J.R. & Michalek, S.M., Am. Rev. Microbiol. 35, 595-638 (1981).
47. Smith, G.E., Trends pharmac. Sci. (in the press).
48. Newbrun, E. Science 217, 418-423 (1982).
49. Sheiham, A. Int. J. Epidemiol. 13, 142-147 (1984).
50. Barrett, M.J. & Williamson, J.J. in Aust. dent. J. 17, 37-50 (1972).
51. Brown, T. in Better Health for Aborigines (eds Hetzel, B. et al.) 97-101 (University of Queensland Press, Brisbane, 1974).
52. Australian Nutrition Foundation, Dent. Outlook 11(2), 47-51 (1985).
53. Fejerskov, O., Antoft, P. & Gadegaard, E., J. dent. Res. 61 (Special Issue), 1305-1310 (1982).
54. von der Fehr, F.R. J. dent. Res. 61 (Special Issue), 1331-1335 (1982).
55. Mansson, B., Holm, A.K., Ollinen, I. & Grahnen, H. Swed. dent. J. 3, 193-203 (1979).
56. Andlaw, R.J., Burchell, C.K. & Tucker, G. J. Caries Res. 16, 257-264 (1982).
57. Mainwaring, P.J. & Naylor, N.M. J. dent. Res. 60, 1140 (1981).
58. Mitropoulos, C.M. & Worthington, H.V. J. dent. Res. 60, 1154 (1981).
59. Downer, M.C. J. dent. Res. 61, 1336-1339 (1982).
60. Palmer, J.D. Br. dent. J. 149, 48-50 (1980).
61. Anderson, R.J. Br. dent. J. 150, 218-221 (1981).
62. Zacherl, W.A. & Long, D.M. J. dent. Res. 58, 227 (1979).
63. Hewat, R.E.T. & Eastcott, D.F., Dental Caries in New Zealand, pp. 75-76, 79 (Medical Research Council of New Zealand, 1955).
Water Fluoridation & Tooth Decay |
Results from the 1986-1987 National Survey of U.S. Schoolchildren |
Excerpt from:
Fluoride: Journal of The International Society for Fluoride Research
Volume 23, No. 2; April, 1990; pp 55-67
Water Fluoridation & Tooth Decay: Results from the 1986-1987 National Survey of U.S. Schoolchildren
by John A. Yiamouyiannis, Ph.D.
Summary:
Data from dental examinations of 39,207 schoolchildren, aged
5-17, in 84 areas throughout the United States are analyzed. Of
these areas, 27 had been fluoridated for 17 years or more (F), 30
had never been fluoridated (NF), and 27 had been only partially
fluoridated or fluoridated for less than 17 years (PF). No
statistically significant differences were found in the decay
rates of permanent teeth or the percentages of decay-free
children in the F, NF, and PF areas. However, among 5-year olds,
the decay rates of deciduous teeth were significantly lower in F
than in NF areas (see results below).
Introduction:
It has become widely accepted among dental and public health professionals, that fluoridation reduces tooth decay by one-half to two-thirds (1,2). However, recent studies by public health dentists in New Zealand, Canada, and the United States have reported similar or lower tooth decay rates in nonfluoridated areas as compared to fluoridated areas (3-6). Moreover, findings in the United States and worldwide show that, over the last 25 years, reductions in tooth decay rates in nonfluoridated areas are comparable to those in fluoridated areas (7-9).
From 1986 to 1987, dentists trained by the U.S. National Institute of Dental Research (NIDR) performed dental examinations on 39,207 schoolchildren, aged 5-17, in 84 areas throughout the United States. This survey allowed a comparison of tooth decay of large numbers of people from a large number of areas, some of which have been fluoridated and some of which have not.
Materials and Methods:
Through the United States Freedom of Information Act, we obtained a printout of the dental records and a list of the 84 areas used in this survey. From these data, we calculated the number of decayed and filled deciduous teeth (dft) and the number of decayed, missing, and filled permanent teeth (DMFT) for each record and entered the resulting data into a computer. All calculations were triple-checked before being entered into the computer and all computer entries were double-checked.
By computer, each record (including the dft and DMFT scores of each student) was placed in the appropriate age group. For each of the 13 age groups, average dft and DMFT rates per child were determined for each of the 84 areas. Age-adjusted DMFT rates for 5- to 17-year olds were calculated by adding the DMFT rates for each of the 13 age groups and dividing by 13 (10).
We obtained the data regarding the fluoridation status of the areas surveyed from Natural Fluoride Content of Community Water Supplies, Fluoridation Census 1969, Fluoridation Census 1975, and Fluoridation Census 1985, all published by the U.S. Public Health Service. In some cases, local authorities were also contacted to determine the fluoridation status of an area.
Average DMFT (and dft) rates for F, NF, and PF groups were calculated for each age. Average-age-adjusted DMFT (and dft) rates for the F, NF, and PF groups were calculated by taking the average of age-adjusted rates for the respective groups (10).
The percentage of "caries-free" children was calculated for each age group for each area. Age-adjusted "caries-free" rates were also calculated. A student was considered to be "caries-free" so long as they had no DMFT or dft. For example, a child who had lost all their teeth and no longer had any left to be decayed or filled would not be recorded as a "caries-free" student.
Through the United States Freedom of Information Act, we also obtained residence data for each of the above schoolchildren which allowed us to calculate tooth decay rates for those in F, NF, and PF areas who had lived at the same residence for their entire life.
The two -talled t-test was used to determine 95% confidence intervals and to determine statistical significance (at the 95% confidence level). A two-sided Wilcoxon rank sum test (11) was used to determine whether there was a statistically significant difference (at the 95% confidence level) in the rank order of DMFT rates of F and NF areas.
Results:
Table 1 presents the number of students examined and the age-adjusted DMFT rate for each of the 84 areas in the order of increasing tooth decay rate. There is no statistically significant difference in the rank order of the age-adjusted DMFT rates of F and NF areas. As can be seen by examination of column 1, there is no clustering of fluoridated areas at the top of the table. In the quartile with the lowest age-adjusted DMFT rates, 9 are non-fluoridated, 3 are partially fluoridated, and 9 are fluoridated. In the quartile with the highest DMFT rates, 5 are nonfluoridated, 10 are partially fluoridated, and 6 are fluoridated. Table 1 also indicates that there is no biased geographical distribution of F and NF areas that is hiding some potential decay preventive effect of water fluoridation.
There is no statistically significant difference between the average DMFT rates for the F and NF groups at any age (Figure 1). The average DMFT rates of the PF groups are higher than those of the F and NF groups at every age with the exception of 14-year olds.
Table 1:
The number of children examined and the average-age-adjusted DMFT, dft, and "caries-free" rates for 5- to 17-year olds in each of the 84 areas in the order of increasing age-adjusted DMFT rate. F refers to areas fluoridated before 1970; PF refers to areas which are only partially fluoridated; PF(x) refers to areas fluoridated in the year "x"; NF refers to areas that are not fluoridated.
Water |
Area |
No. |
DMFT |
dft |
Caries-free |
NF | Buhler, KS | 543 | 1.229 | 0.810 | 44.7% |
F | El Paso, TX | 451 | 1.321 | 0.777 | 43.5% |
NF | Brooklyn, CT | 410 | 1.420 | 0.693 | 47.6% |
F | Richmond, VA | 475 | 1.435 | 0.715 | 45.6% |
F | Ft. Scott, KS | 491 | 1.442 | 0.774 | 38.2% |
F | Prince George, MD | 443 | 1.491 | 0.539 | 48.0% |
NF | Cloverdale, OR | 354 | 1.494 | 0.872 | 40.4% |
PF(71) | Alliance, OH | 467 | 1.584 | 0.549 | 44.6% |
NF | Martin, Co., FL | 440 | 1.587 | 0.677 | 41.0% |
F | Andrews, TX | 455 | 1.588 | 0.893 | 35.8% |
NF | Coldspring, TX | 406 | 1.589 | 1.144 | 33.8% |
F | Tulsa, OK | 504 | 1.602 | 1.075 | 35.5% |
NF | Palm Beach, FL | 476 | 1.613 | 0.896 | 34.5% |
PF | Hocomb, MO | 558 | 1.628 | 0.883 | 40.3% |
NF | Kitsap, WA | 564 | 1.635 | 0.769 | 42.9% |
F | St. Louis, MO | 491 | 1.638 | 0.711 | 39.1% |
PF (82) | Houston, TX | 488 | 1.662 | 0.819 | 41.8% |
F | Clarksville, IN | 428 | 1.678 | 0.747 | 40.4% |
NF | Grand Island, NE | 535 | 1.719 | 0.789 | 40.7% |
F | Ft. Stockton, TX | 415 | 1.722 | 0.891 | 33.4% |
NF | San Antonio, TX | 422 | 1.736 | 0.895 | 39.3% |
F | Cherry Creek, CO | 441 | 1.757 | 0.727 | 36.5% |
F | Tuscaloosa, AL | 475 | 1.809 | 0.963 | 32.0% |
PF | Marlon Co., FL | 545 | 1.817 | 0.944 | 28.8% |
F | Cleveland, OH | 486 | 1.819 | 0.715 | 39.9% |
NF | Allegany, MD | 458 | 1.834 | 0.735 | 38.3% |
PF (78) | Norwood, MA | 434 | 1.841 | 0.640 | 39.9% |
F | Alton, IL | 511 | 1.859 | 0.843 | 37.6% |
NF | Shamokin, PA | 462 | 1.861 | 1.023 | 32.2% |
NF | Lodi, CA | 573 | 1.878 | 1.197 | 33.0% |
PF | Bullock Creek, MI | 472 | 1.879 | 0.766 | 36.7% |
PF (82) | Marlboro, MA | 386 | 1.885 | 0.613 | 40.8% |
PF (81) | Allen, TX | 445 | 1.905 | 0.674 | 38.7% |
F | San Francisco, CA | 456 | 1.908 | 1.031 | 36.3% |
NF | E. Orange, NJ | 401 | 1.909 | 0.796 | 38.0% |
PF (71/60) | Lincoln/Sudbury, MA | 436 | 1.923 | 0.758 | 37.8% |
NF | Conejo, CA | 620 | 1.930 | 0.811 | 41.7% |
NF | Lakewood, NJ | 450 | 1.933 | 0.698 | 38.0% |
F | New York City-2 | 336 | 1.953 | 0.812 | 34.9% |
PF | Bethel, WA | 540 | 1.958 | 1.072 | 34.3% |
F | Beach Park, IL | 518 | 1.970 | 0.878 | 35.2% |
PF | Rising Star, TX | 370 | 1.971 | 0.909 | 28.7% |
F | Philipsburg, PA | 499 | 1.983 | 0.982 | 33.2% |
F | Lanett, AL | 503 | 1.994 | 0.978 | 31.9% |
PF (82) | Plainville, CT | 436 | 2.006 | 0.795 | 39.3% |
NF | Wichita, KS | 496 | 2.036 | 0.878 | 33.5% |
NF | Newark, NJ | 494 | 2.038 | 0.869 | 35.9% |
PF | Knox Co., TN | 530 | 2.056 | 1.152 | 31.3% |
NF | Los Angeles, CA | 540 | 2.063 | 1.039 | 33.0% |
F | Pittsburgh, PA | 415 | 2.064 | 0.781 | 34.1% |
PF (70) | Lincoln, NE | 476 | 2.076 | 0.825 | 31.5% |
NF | Newton, KS | 464 | 2.083 | 1.225 | 31.1% |
PF | Lakeshore, MI | 486 | 2.088 | 0.781 | 32.6% |
NF | New Paltz, NY | 350 | 2.110 | 0.751 | 34.8% |
F | Bemidgl, MN | 485 | 2.124 | 1.001 | 29.3% |
NF | Alpine, OR | 397 | 2.133 | 0.974 | 34.7% |
NF | Canon City, CO | 463 | 2.160 | 1.118 | 33.1% |
NF | Wyandank, NY | 396 | 2.161 | 0.828 | 34.7% |
NF | Milbrook, NY | 332 | 2.179 | 0.716 | 32.2% |
NF | Chowchilla, CA | 551 | 2.181 | 1.073 | 33.0% |
F | New York City-1 | 503 | 2.190 | 0.627 | 37.9% |
PF (82) | Baltic, SD | 487 | 2.193 | 0.974 | 27.8% |
PF (71/74) | Blue Hill, NE | 480 | 2.218 | 0.855 | 29.6% |
NF | Crawford, PA | 492 | 2.222 | 0.996 | 28.5% |
PF (74) | New Orleans, LA | 459 | 2.251 | 0.953 | 27.4% |
PF (70) | Memphis, TN | 464 | 2.253 | 0.763 | 33.1% |
PF | Madison Co., MS | 493 | 2.259 | 1.455 | 26.4% |
F | Milwaukee, WI | 478 | 2.349 | 0.909 | 32.1% |
NF | Tooele, UT | 519 | 2.372 | 1.458 | 24.3% |
NF | Chicopee, MA | 453 | 2.389 | 0.862 | 34.2% |
PF | Cambria, PA | 532 | 2.460 | 1.039 | 27.1% |
PF (75) | Springfield, VT | 444 | 2.489 | 0.838 | 32.1% |
F | Dearborne, MI | 491 | 2.496 | 1.167 | 26.3% |
F | Maryville, TN | 466 | 2.512 | 1.287 | 22.9% |
PF (81) | Taunton, MA | 445 | 2.515 | 0.903 | 31.0% |
F | Greenville, MI | 556 | 2.558 | 1.191 | 25.3% |
PF | Hart/Pentwater, MI | 455 | 2.584 | 1.344 | 24.1% |
F | Philadelphia, PA | 463 | 2.649 | 0.824 | 26.0% |
PF | Sup. Union #47, VT | 487 | 2.710 | 0.907 | 28.1% |
NF | Cutler/Oroal, CA | 528 | 2.796 | 1.742 | 19.2% |
F | Brown City, MI | 512 | 2.972 | 1.229 | 22.5% |
PF (83) | Lawrence, MA | 339 | 3.012 | 1.262 | 17.6% |
NF | State of Hawaii | 293 | 3.294 | 1.375 | 23.9% |
PF | Concordia, Co., LA | 424 | 3.767 | 1.508 | 12.4% |
Figure 1:
Tooth decay in fluoridated (F), partially fluoridated (PF), and non-fluoridated (BF) areas: Permanent Teeth.
Table 2:
Average-age-adjusted DMFT
rates for 39,207 U.S. schoolchildren and 17,336 life-long
resident schoolchildren in 84 areas throughout the United States.
Standard deviations are given in parentheses.
Total | Life-long | ||||
No. of Areas | No. of Students | DMFT | No. of Students | DMFT | |
Fluoridated | 27 | 12,747 | 1.96 (0.415) | 6,272 | 1.97 (0.465) |
Partially Fluoridated | 27 | 12,578 | 2.18 (0.485) | 5,642 | 2.25 (0.470) |
Nonfluoridated | 30 | 13,882 | 1.99 (0.408) | 5,422 | 2.05 (0.517) |
Figure 2A:
Tooth decay in residents of fluoridated (F), nonfluoridated (NF), and partially fluoridated (PF) areas who lived their entire life in the same household.
* Read the Chemical and Engineering News (1989) article "New Studies Cast Doubt on Fluoridation Benefits" which discusses this study.
References:
1) Green, J.C., Louie, R. and Wycoff, S.J.: Preventive Dentistry I. Dental Caries. J. Amer. Med. Assn., 262:3456-3463, 1989.
2) Szpunar, S.M. and Burt, B.A.: Dental Caries, Fluorosis and Fluoride Exposure in Michigan Schoolchildren. J. Dent. Res., 67:802, 1988.
3) Colquhoun, J.: Influence of Social Class and Fluoridation on Child Dental Health. Community Dent. Oral Epidemiol., 13:37-41, 1985.
4) Colquhoun, J.: Child Dental Health Differences in New Zealand. Community Health Studies, 11:85-90, 1987.
5) Gray, A.S.: Fluoridation: Time for a New Baseline? J. Canadian Dent. Assoc., 53:763-765, 1987.
6) Hildebolt, C.F., Elvin-Lewis, M., Molnar, S., McKee, J.K., Perkins, M.D. and Young, K.L.: Caries Prevalences Among Geochemical Regions of Missouri. Amer. J. Physical Anthropol., 78:79-92, 1989.
7) Diesendorf, M.: The Mystery of Declining Tooth Decay. Nature, 322:125-129, 1986.
8) Johnston, D.W., Grainger, R.M. and Ryan, R.K.: The Decline of Dental Caries in Ontario School Children. J. Canadian Dent. Assoc., 52:411-417, 1986.
9) Luoma, A-R. and Ronnberg, K.: Twelve-Year Follow-up of Caries Prevalence and Incidence in Children and Young Adults in Espoo, Finland. Community Dent. Oral Epidemiol., 15: 29-32, 1987.
10) Hill, A.B.: Medical Statistics. Hodder and Stoughton, London, 1977, p. 183. While the numerous age-specific comparisons of dental health of children at different ages provide the best evidence, it is occasionally desirable to have a summary rate to enable an overall comparison of different populations. For this purpose, we have used the age-standardized or age-adjusted rates, in order to avoid giving disproportionate weighting to larger numbers of children from one particular age-group that would tend to distort the summary figure. In using these rates, a standard population must be chosen. The one most commonly used is the hypothetical population with equal populations at each age group, which merely results from taking an arithmetic mean of the age-specific tooth decay rates measured. In the above reference, Austin Bradford Hill addresses this method in a discussion of the handling of mortality rates under a section titled "The Equivalent Average Death-Rate." Analogously, equal weights were given to each of the 84 geographical areas to prevent a distortion which might be induced by the variation of the area sample sizes, since certain geographical areas have characteristically higher (or lower) tooth decay rates than others.
11) Wilcoxon, F., Katti, S.K. and Wilcox, R.A.: Critical Values and Probability Levels for the Wisconsin Rank Sum Test and the Wilcoxon Signed Rank Test. Selected Tables in Mathematical Statistics, Markham Publishing Co., Chicago, 1:197, 201, 1970.
After 50 Years, Fluoride Supplements have Never been Approved by the FDA |
N.J. Assemblyman Asks for Senate Hearing |
NEW JERSEY GENERAL ASSEMBLY
John V. Kelly | COMMITTEES | |
Assemblyman, 36th District | Chair | |
Bergen-Essex-Passaic Counties | Housing Committee | |
371 Franklin Avenue, 2nd Floor | New Jersey Fire Safety Commission | |
Nutely, NJ 07110 | Member | |
(973) 667-6123 | Appropriations Committee | |
Fax (973) 667-9614 | Governor's Landlord-Tenant Task Force | |
Ellis Island Advisory Committee |
August 14, 2000
Senator Robert Smith,
Chairman
Environment and Public Works Committee
c/o John Pemberton
307 Dirkson Senate Office Building
Washington D.C. 20510-0001
Dear Senator Smith:
In 1992, the New Jersey Department of Health released a study suggesting an association between fluoridated water and osteosarcoma in young males. The New Jersey study was undertaken in response to a national epidemiology study (Hoover 1991) and a National Toxicology program study (1990) linking fluoride and osteosarcoma.
Upon receiving this study, I immediately contacted the American Academy of Pediatric Dentistry (AAPD) and asked them to send me the studies supporting the safety and effectiveness of fluoride supplements. (Fortunately, New Jersey has little fluoridated water. As a result, pediatricians in our state prescribe fluoride supplements -- drops for infants and tablets for children.) I was promised the studies - they never came. When I pressed the AAPD, they admitted they had no such studies and informed me the studies could be obtained from the National Institute of Dental Research (NIDR). They assured me they would forward the studies. Again, they never came. NIDR acknowledged they did not have any studies. The NIDR recommended I obtain the studies directly from the FDA since that agency was responsible for approving these products.
After filing a FOIA and waiting six months, I was stunned when I was advised by the FDA that fluoride supplements were not approved by the FDA (emphasis in original). Incredibly, in fifty years, no one has ever bothered submitting a petition to the FDA to have these products approved!
The water fluoridation debate has been raging for fifty years. The dose recommended for water fluoridation when adjusted for weight is the same dose recommended for prescription supplements. However, no clinical trials have been conducted and submitted to the FDA to demonstrate the effectiveness of ingesting fluoride.
So, the question remains, if the FDA does not recognize the safety and effectiveness of fluoride supplements, how can we even consider fluoridating water?
Toxicology studies and clinical trials of fluoride supplements submitted to the FDA would have been the simplest, clearest and lawful way of demonstrating the safety and effectiveness of ingesting fluoride. There is no reason to debate epidemiology studies. Simply submit fluoride supplement studies to the FDA and we will know whether fluoride is safe and effective.
Of course, the reason this has not happened in half a century is because the promoters of fluoride supplements dare not go anywhere near the FDA, fully aware that they could never meet the requirements of demonstrating safety and effectiveness. Rejection by the FDA of petitions for fluoride supplements would be the death knell for water fluoridation, so the FDA and the law are simply ignored.
It is my understanding that in 1975, the FDA issued a regulatory letter asking manufacturers to remove fluoride supplements from the market. To date, the FDA has not responded to my inquiry asking for clarification of their actions in 1975. Also, in 1993 I petitioned the FDA to enforce the law and remove children's fluoride supplements from the market. The FDA has ignored my repeated requests.
At best, fluoride supplements are a waste of precious health care dollars. At worst, they are causing real harm to our infants and children.
I urge you to hold hearings on this issue. I also urge you to demand that the FDA enforce the law and remove these unapproved products from the market.
Sincerely,
John V. Kelly
Assemblyman District 36
What Other Governments have to Say about Fluoridation
In response to the United States' most ardent proponent of fluoridation, Michael Easley, (Director, National Center for Fluoridation Policy and Research), FAN has listed the following statements from governments which have rejected fluoridation. It is interesting and important to note, that despite claims by proponents such as Easley that fluoridation reduces cavities by 40 to 60%, the following countries on average have just as healthy teeth as the highly fluoridated United States (i.e. they do not have more cavities). Moreover, since these countries don't consume fluoride everyday in their drinking water, they have less incidence of dental fluorosis (white spots and mottling of the teeth) than people of the United States.
Despite the fact, however, that non-fluoridated Western Europe and Japan have the same levels of cavities as Americans, Easley somehow feels there can be "no controversy" surrounding fluoridation. In a recent paper written by Easley, he argues against debating with fluoridation opponents (whom he calls "fluorophobics.") According to Easley (1999), proponents shouldn't agree to public debates because "debates give the illusion that a scientific controversy exists when no credible people support the fluorophobics view." "Like parasites," Easley adds, "opponents steal undeserved credibility just by sharing the stage with respected scientists who are there to defend fluoridation."
Easley seems unable to fathom how people, such as US consumer advocate Ralph Nader, can be opposed to fluoridation. More troubling is that Easley argues that dentists and physicians should not be allowed to speak out against this policy. As he puts it, "a most flagrant abuse of the public trust occasionally occurs when a physician or a dentist, for whatever personal reason, uses their professional standing in the community to argue against fluoridation, a clear violation of professional ethics, the principles of science, and community standards of practice."
FAN awaits to see if Easley draws suit against the Governments of Japan, Belgium, Germany, Netherlands, France, Norway, Sweden, Denmark, Italy, Greece, and Luxembourg for unethically rejecting fluoridation. It would be hard to see, however, how he could claim wrongdoing to their peoples since they have just as few cavities as the the 62%+ fluoridated United States.
(The full photocopied letters from which the following statements are taken can be accessed at: www.fluoridation.com/c-country.htm)
Japan:
"Japanese government
and local water suppliers have considered there is no need to
supply fluoridated water to ALL users because 1) impacts of
fluoridated water on human health depends on each human being so
that inappropriate application may cause health problems of
vulnerable people, and 2) there is other ways for the purpose of
dental health care, such as direct F-coating on teeth and using
fluoridated dental paste and these ways should be applied at
one's free will." (Toru Nagayama,
Environment Agency, Government of Japan, Tokyo, March 8, 2000).
Belgium:
"This water treatment has never been of use in Belgium and
will never be (we hope so) into the future." (Chr.
Legros, Directeur, Belgaqua, Brussels, Belgium, February 28,
2000).
Denmark:
"We are pleased to
inform you that according to the Danish Ministry of Environment
and Energy, toxic fluorides have never been added to the public
water supplies." (Klaus Werner Royal Danish
Embassy, Washington DC, December 22, 1999).
Norway:
"In Norway we had a
rather intense discussion on this subject some 20 years ago, and
the conclusion was that drinking water should not be
fluoridated." (Truls Krogh & Toril
Hofshagen, Folkehelsa Statens institutt for folkeheise (National
Institute of Public Health) Oslo, Norway, March 1, 2000).
Sweden:
"Drinking water
fluoridation is not allowed in Sweden...New scientific
documentation or changes in dental health situation that could
alter the conclusions of the Commission have not been
shown." (Gunnar Guzikowski, Chief Government
Inspector, Livsmedels Verket -- National Food Administration
Drinking Water Division, Sweden, February 28, 2000).
Germany:
"In the former
Democratic Republic of Germany (DDR) in several districts the
drinking water was fluoridated but after the unification of both
German states in 1990 fluoridation was stopped. In the Federal
Republic of Germany there was in about 1952 a drinking water
fluoridation experiment. But it was stopped after one or two
years." (Dr. K. Ewing (sp?),
Geschaftszeichen (Bei allen Antworten bitte angeben), Bonn,
Germany, February 11, 2000).
Finland:
"We do not favor or
recommend fluoridation of drinking water. There are better ways
of providing the fluoride our teeth need." (Paavo
Poteri, Acting Managing Director, Helsinki Water, Finland,
February 7, 2000).
Austria:
"Toxic fluorides have never been added to the public water supplies in Austria." (M. Eisenhut, Head of Water Department, Osterreichische Yereinigung fur das Gas-und Wasserfach Schubertring 14, A-1015 Wien, Austria, February 17, 2000).
Is water fluoridation the
saviour of all dental evil or is fluoride a dangerous poison
which makes money for the dental industry? Joanna Blythman
investigates
Publication Date: Sep 3 2000
To most people, fluoride is a wholly beneficial chemical with no downside whatsoever. Its remarkably favourable public image is based on our trust of the dental profession which has been telling us since the 1950s that fluoride is good for our teeth and advising us to brush them with fluoride toothpaste and swallow fluoride tablets. Fluoride is the dental magic bullet for deprived urban children whose teeth are rotten at an absurdly early age. Fluoridate their drinking water and hey presto, Blackhill kids get Bearsden teeth, even if they dont possess a toothbrush and live on sugary fizzy drinks. But a growing body of international scientific and environmental opinion sees fluoride as nothing more than a poisonous pollutant, profitably and misleadingly rebadged as the scourge of dental caries. Discomfitingly for the fluoride lobby, evidence to support these claims is building up as studies link it with adverse health effects including tooth discolouration, lowered IQ, increased perinatal mortality and birth defects, bone cancer, osteoporosis and hip fractures.
Even leading dental authorities are having second thoughts. Aubrey Sheiham, professor of community dental health at University College London, says: "I have gone cool on water fluoridation. Fluoride does have a definite negative effect on teeth. Also the dental profession's concentration on fluoride has let sugar off the hook." Could it be that fluoride is one of the greatest chemical blunders of the last century? Fluoride entered the public health frame in the 1930s when an American doctor noted that the teeth of children in areas with a high natural calcium fluoride level in water were stained and discoloured, a condition named fluorosis. It was no surprise that fluoride damaged teeth. In 1936, the American Dental Journal condemned fluoride as "a general protoplasmic poison the most important symptoms of chronic poisoning known at present are mottling of the teeth and interference with bone formation". Until then, it had been commonly used as a rat poison. Fluoride is still classified as an "extremely toxic" substance, rated between 4 and 5 on a toxicity scale of 1-6, more poisonous than lead and almost as poisonous as arsenic. Not the sort of thing you want to ingest. Fluoride is not a nutrient, you do not need it in your diet. But doctors and dentists were persuaded that the children with fluorosis had fewer dental caries, and therefore, that fluoride prevented decay. Mottled teeth were just a small cosmetic price to pay for this dental breakthrough. And to this day fluoridation is still pursued with missionary fervour. "We're talking massive improvements to tooth health and less avoidable pain and misery all by implementing a safe and effective public health measure," says Sheila Jones, spokeswoman for the British Fluoridation Society, a government-funded body which promotes fluoridation.
This government has targeted four areas of poor tooth health it wants to see fluoridated - Northwest England, Northern Ireland, the West of Scotland and Inner London. Over the past three decades, Northern Ireland and the North of England have rejected fluoridation four times. In a landmark court battle in 1983, Lord Jauncey ruled that Strathclyde was exceeding its legal authority when it tried to fluoridate its water. London mayor, Ken Livingstone, has said that he will oppose it too. Others have tempered their traditional unbridled advocacy of fluoride with more measured warnings which reflect its toxic status. "In the past 10 years we have been aware that children do have an increased risk of adverse effects and are recommending that when brushing teeth, only a pea-sized drop of fluoride toothpaste should be used and that parents supervise brushing to make sure that children spit it out," says Dr John Beal of the British Dental Association. What otherwise might they be swallowing? Fluoride is a by-product of phosphate fertiliser or aluminium production and a dangerous pollutant. "Companies cannot by law dump this material in the environment but they are allowed to sell it to public water utilities where it is diluted down in the water supply," says Dr Paul Connett, an international expert on environmental toxins. He states that whenever fluoride is tested in laboratories, usually on rats, a pharmaceutical grade of sodium fluoride is used with distilled or double-deionised water and this is entirely different from the substance put into the public water supply which is hexafluorosilicic acid, a toxic soup of silicofluorides and a number of other contaminants from the phosphate process which commonly include arsenic, cadmium and radionuclides. According to the BDA, such claims are "complete, unmitigated drivel". "Fluoride from phosphate manufacture is just a convenient type of recycling which meets strict government safety standards, monitored by the Drinking Water Inspectorate," says Beal.
But can there ever be a
"safe" level for any poison? The "optimal"
level for fluoride in water was set at one part per million back
in 1945, with no allowance made for the cumulative effect of
other sources of fluoride such as fluoridated dental products,
soft drinks and processed foods. Nor have the possible
synergistic cocktail effects of fluoride with other chemicals we
ingest been taken into account.
While the BDA insists that "fluoridation could reduce decay
in cities like Glasgow by a half", other European countries
remain unconvinced. Only the UK, Ireland and Spain fluoridate
their drinking water in some areas. It is the same story
internationally. The Japanese government's position, for example,
is that wholesale water fluoridation can cause health problems
and that individuals are at liberty to use a fluoride toothpaste
if they wish. These days, non-fluoridated Western Europe and
Japan have the same, or in some cases fewer, dental cavities than
the US. Meanwhile in the 62%-fluoridated US, fluorosis, which
ought to be rare, is running at between 20% to 80%. More than 50
US towns and cities have stopped fluoridation since 1990.
Sheiham says: "When I worked in the US, the first thing I
noticed was what nice white teeth Americans had. But tooth
whitening is an initial sign of low-score fluorosis. The staining
comes later with the higher scores. Ironically, it is the
middle-class children that are most badly affected by excess
fluoride because they also use fluoride toothpaste."
Increasingly more scientists seem to agree that if there is any
benefit to fluoride at all, it comes from topical application
(toothpaste), not indiscriminate and ill-targeted mass
fluoridation which could cause problems for vulnerable groups
such as the elderly, diabetics, people with vitamin and mineral
deficiencies and cardiovascular or kidney problems. And what
about the perfectly healthy population? Why ingest a known toxin
on a lifetime basis just because some children suffer from too
much tooth decay? Why not add aspirin to water in order to
prevent heart disease and strokes in the elderly, or spray
steroids into the air because some people get asthma?
British opponents of
fluoridation point out that only about 3% of the global
population is artificially fluoridated and that the strong
American drive to promote the practice has been spectacularly
unsuccessful. "The trick is to make people think that they
are somehow behind the times and should feel guilty for depriving
their children of this miracle-working pollution," says Jane
Jones, campaign director of the National Pure Water Association.
The fluoride debate is certainly calling into question the
integrity of the dental research community. Can we trust
dentists? And even if we are talking about those well-intentioned
dentists who have simply subscribed to a professional orthodoxy,
do they see the wider health picture? "The public have been
sold a Janet and John story about fluoride," says Jones. She
makes the ultra-cynical observation that dentists have a
financial interest in promoting fluoride because they can make
more money covering up the staining of fluorosis than carrying
out extractions or fillings. Recently the credibility of the
British Dental Association took a knock when it gave its official
accreditation to a soft drink - Ribena Tooth Kind - which claimed
it was "safe for teeth". (The BDA makes tens of
thousands of pounds each year from product accreditation.) The
Advertising Standards Authority found that these claims were
misleading. Now the BDA defends its accreditation on the grounds
that that it was only saying that Ribena Tooth Kind was less
harmful than other sweet drinks and not suggesting that there was
no danger of decay. Thisdebacleillustratesthesomewhat ambivalent
relationship that exists between the advocates of fluoride and
the sugar industry. Sugar and the corrosive acids in fizzy drinks
are the number one cause of tooth decay and their effect is most
damaging amongst deprived urban children with poor diets who do
not take care of their teeth. Yet sugar overconsumption in such
communities is often met with shoulder-shrugging and patronising
tolerance while Nanny State interventionism is advocated in the
form of water fluoridation.
"Fluoride has been found to be effective over 40 years in
improving dental health by 60%. It is a much more realistic way
of tackling tooth decay than approaching the manufacturers of
sugary drinks," says Margie Taylor, consultant in Dental
Public Health in Lanarkshire. Now the University of York has been
funded by the government to come up with a "once and for
all" review of the science around fluoride. It is due to
report in two weeks and expected to conclude that fluoride is
safe and effective. "They set narrow criteria for the review
which excluded all biochemistry and animal studies, mathematical
models and the cocktail effect. What's more they have been
looking at areas with naturally high calcium fluoride, not the
artificial product that is put into water," explains Jones.
But the public's current disillusionment with tame government
scientists in the wake of BSE is high. Consumers were assured by
august committees that the risk to humans was "remote".
It seems unlikely that the York review will silence the long,
persistent and mounting opposition to fluoridation.