This is Paul Connett’s response to Ken Perrott’s last article Fluoridation debate: Why I support fluoridation – 2nd reply to Connett.
For Ken Perrott’s original article see - Fluoride debate: Why I support fluoridation.
When is Ken going to present his case for fluoridation?
In his thread Ken has had three opportunities to present the Case for Fluoridation, but he seems to be content to nibble around the edges. His stating over and over again that the fluoride ion is a natural constituent of apatites doesn’t get us very far. I was expecting by now that Ken would have tackled three basic questions head on:
1) Is it Ethical?
2) Is it Effective?
3) Is it Safe?
I was expecting the ethical case to be tackled with rigor, but Ken quickly dismissed the central question of whether fluoridation was medical treatment as simply a matter of semantics. Clearly, if fluoridation is medical treatment or even simply human treatment, it violates the individual’s right to informed consent for such treatment. So simply declaring this to be a matter of semantics dodges a very important issue – and for many opponents of fluoridation the central issue.
So let me ask Ken if he will accept this two-part definition of a medicinal product from the European Union Directive 2004/27/EC:
(a) Any substance or combination of substances presented as having properties for treating or preventing disease in human beings; or
(b) Any substance or combination of substances which may be used in or administered to human beings either with a view to restoring, correcting or modifying physiological functions by exerting a pharmacological, immunological or metabolic action, or to making a medical diagnosis.
No RCTs after 68 years
As for the second and third questions I was expecting Ken to layout the scientific studies that had convinced him that fluoridation was both safe and effective. Ideally, one would have wanted him to give a link to a randomized controlled trial (RCT) establishing the effectiveness and assessing the safety of this practice. This after all is the gold standard for such matters. However, after 68 years of this practice this has not been attempted.
Failing an RCT one would have wanted to see Ken identify the best quality studies that have convinced him that the practice he advocates and defends actually works to a meaningful extent against a background of other sources of fluoride, and does not present any dangers – especially to those he particularly wants to help, children from low-income families.
Moreover, since this is a practice being forced on millions of people – and in thousands of cases against their expressed opposition –one has the right to anticipate that proponents would be able produce the highest quality studies that overwhelmingly demonstrate their case. With a forced measure like this, one would have anticipated little room for any doubt about whether it worked or not, and by which mechanism it worked. Moreover, should harm be demonstrated at some higher dose level, one would have anticipated that proponents would be able show that the margin of safety would be so high that the even the most vulnerable individuals in society would be protected no matter how much water they drank and no matter how much fluoride they got from other sources.
So where is this overwhelming evidence of effectiveness and safety Ken?
Ken has ducked key discussions and questions
So far Ken has provided little evidence to demonstrate any of the above reasonable expectations for such a practice. He has even ducked key discussions on the difference between concentration (mg/liter), dose (mg/day) and dosage (mg/kg/day). Comparisons based only on concentrations – and not on dose or dosage – such as used by Siegal and Sparrow in their respective diagrams, are seriously limited if not meaningless. Nor has he addressed even the need for a margin of safety analysis when harm has been found at high doses. Ken does not deny that harm (e.g. hip fractures and lowered IQ) has been found only that the concentration (ignoring the issue of dose) was too high to be of significance
This refusal to lay out his case in comprehensive scientific terms was most clearly revealed in his response to two things I asked for in my last posting:
a) Where is the body of scientific evidence that indicates that fluoride is not a neurotoxicant?
b) Provide a list of primary studies that have most convinced him that fluoridation is safe for the bottle-fed infant and lifelong exposure for the adult.
As far as a) is concerned, I offered a large body of evidence that fluoride was a neurotoxicant:
Over 40 animal studies show that prolonged exposure to fluoride can damage the brain.
19 animal studies report that mice or rats ingesting fluoride have an impaired capacity to learn and remember.
12 studies (7 human, 5 animal) link fluoride with neurobehavioral deficits
3 human studies link fluoride exposure with impaired fetal brain development
37 out of 43 published studies show that fluoride lowers IQ, of which 27 were part of a meta-analysis conducted by a team from Harvard (Choi et al.) (www.fluoridealert.org/issues/health/brain)
Contrary to arguments by proponents the vast majority of these IQ studies were carried out at concentrations which offered little or no margin of safety to protect all children in a large population drinking uncontrolled amounts of fluoridated water and getting fluoride from several other sources, including sources unlikely to be available to many of the children in these studies (e.g. fluoridated toothpaste and bottle-feeding with formula made up with fluoridated tap water). Up to 10 of the studies in the Choi analysis had levels in the high fluoride village of 3 ppm or less.
So that was the weight of evidence on my side of the pan scale, it is only after seeing what Ken can put in the pan on his side of the scale that independent observers can make a scientific judgment on the true weight of evidence (see more below). Only then can we know if it is wise to ignore the many red flags being waved on this issue.
But Ken ignored this reasonable request preferring instead to rehash his criticisms of just Xiang’s work.
The need for a weight of evidence approach
What we need here – not only on neurological effects but for all the health concerns – is a weight of evidence approach. In this approach the quality, quantity, and relevance of all available evidence should be weighed and balanced (synthesized) to arrive at a conclusion. For the question of fluoridation, some of that evidence comes from animal experiments, some from epidemiological studies, some should come from RCTs on effectiveness (which amazingly -as indicated above – don’t exist for fluoride), some from medical case reports, some from basic biological/chemical/physical knowledge, and some from ethical considerations. This is what the National Research Council did in its 2006 report (except the NRC didn’t examine the ethical issues), and what we tried to do in our book and what I had hoped Ken would have attempted in presenting his Case For Fluoridation.
As far as b) is concerned, this was Ken’s reply:
Paul wants me “to list the primary studies that you have read which most convinced you that fluoridation is both safe for the bottle-fed baby and for the adult over lifelong exposure.” In thinking about this I have concluded it is a strange request because I don’t think creative scientists think that mechanically.
My concepts and ideas derive from multiple sources – I never put my eggs all in one basket as it were. I can find I am impressed by something in a paper which also has something which doesn’t impress me. Consequently I take what I can from wherever I can and try to critically understand what I read.
It’s a bit like that with people. You have to accept them warts and all and avoid the immaturity of placing anyone on a pedestal – a sure way to later find they have feet of clay.
So unfortunately I cannot satisfy Paul’s request. He will have to deal with the actual arguments I put forward.
I am sorry Ken, I don’t mean to be rude but I find this response a total waffle. If you have the science to support the safety of fluoridation – and can discount many of the health concerns that I and others have raised – then you should be able to present that case using primary health studies, and preferably primary health studies carried out in NZ. You should then be able to buttress that with all the other scientific information available and then apply a weight of evidence analysis as discussed above. After all it is a practice you want to see imposed on others; as such it is your case to win. If you can’t do that then your support of water fluoridation is highly suspect and amounts to little more than posturing. So I would like to tighten up this discussion and ask you some very specific questions.
A few very specific questions pertaining to health concerns
At the outset, before I lay out these questions, I have to acknowledge the fact that in some respects this is not a level playing field for opponents and proponents of fluoridation. It may appear that I am demanding too much from Ken. I admit that the matter is intrinsically unfair. For a critic of fluoridation it is only necessary to produce one ugly fact – one health concern that has not been resolved – to put the practice into question. I can produce several.
On the other hand a proponent of a measure that is being forced on millions of people should be on top of every health concern. A proponent should be able to demonstrate (or at least feel satisfied) that every health concern has been addressed in such a way (i.e. via careful study) so as to leave no residual concerns. It is tough burden but is the nature of the beast when proposing or supporting a health measure that is forced on millions of people.
The shocking fact is that many health questions were unresolved when fluoridation was launched in 1945 and endorsed by the US Public Health Service in 1950 (see chapters 9 and 10 in The Case Against Fluoride…).
There are many health concerns that have not been carefully studied
I am afraid that the sad truth is that there are many serious health concerns with respect to swallowing fluoride and lifelong exposure to fluoridated water and other sources in our daily lives that have simply not been carefully studied in fluoridated countries and thus still unresolved. The York Review (McDonagh et al., 2000) reached this conclusion in 2000, as did the chairman, John Doull, of the NRC (2006) review. In an interview in Scientific American (Jan, 2008), the NRC chairman was quoted as saying:
“What the committee found is that we’ve gone with the status quo regarding fluoride for many years—for too long really—and now we need to take a fresh look . . .In the scientific community people tend to think this is settled. I mean, when the U.S. surgeon general comes out and says this is one of the top 10 greatest achievements of the 20th century, that’s a hard hurdle to get over. But when we looked at the studies that have been done, we found that many of these questions are unsettled and we have much less information than we should, considering how long this [fluoridation] has been going on.” (Fagin, 2008).
Doubtless Ken will point out that Doull has since made a statement supporting water fluoridation, which has been circulated by proponents. However, his own personal opinion of water fluoridation does not diminish in any way his comments on the poor quality of the research on this matter. What is even more distressing is that since the NRC (2006) report was published practically none of the research recommended by the committee has been carried out.
Ken will find out for himself how poorly fluoridated countries – especially New Zealand – have investigated the health concerns pertaining to fluoridation, if he opens his parachute and seeks answers to the very specific questions I have listed below.
My specific questions for Ken pertaining to health concerns
1) Can you find studies that have convinced you that lifelong exposure to fluoridated water and other daily sources of fluoride (i.e. total daily dose of fluoride) is not increasing the risk of arthritis or arthritic-like symptoms, which have been identified as being the first symptoms of fluoride toxicity in research on skeletal fluorosis (see, e.g., Boillat 1980; Czerwinski 1988; Hileman 1988). These symptoms occur long before we reach bone levels that cause crippling skeletal fluorosis, the only end point considered by the US EPA when they determined the safe drinking water standard for fluoride in 1986 (i.e. 4 ppm).
2) Repeating two earlier requests, can you produce the studies that have convinced you that long term exposure to fluoridated water and other common sources of fluoride causes no damage to individuals with impaired kidney function?
3) Can you find studies that have convinced you that exposure to fluoridated water and other daily sources of fluoride (i.e. total daily dose of fluoride) is not increasing the risk of lowered thyroid function, including among those with suboptimal iodine intake (Galleti and Joyet, 1958; Lin 1991). This is an especially relevant question in light of the increase in iodine deficiency seen in the U.S. and other western nations over the past 30 years, as well as the large increases in the incidence of hypothyroidism. Lowered thyroid function would be one explanation for lowered IQ and would also explain the delayed eruption of the teeth for which there is some evidence.
4) Can you find any study that has refuted the key finding by Bassin et al., 2006, that there appears to be an age-specific nature to the risk of boys developing osteosarcoma when exposed to fluoride? In a matched case-control study Bassin found that boys exposed to fluoridated water in their 6th to 8th years had a 5-7 fold increased risk of succumbing to osteosarcoma by the age of 20. Note: The much-anticipated study by Bassin’s thesis advisor Chester Douglass (Kim et al, 2011) failed to address Bassin’s central thesis concerning the age-specific nature of the risk despite prior claims that it would (Joshipura and Douglass, 2006)
5) Can you find any attempt by any health agency in any fluoridated country to investigate in a scientific manner a) the many anecdotal reports, b) case studies by Waldbott, 1955; Shea et al., 1967; Grimbergen, 1974; Petraborg, 1974, 1977; and c) a clinical trial by Feltman, 1956 and Feltman and Kosel, 1961, that suggest that some individuals (may be 1% of the population) are very sensitive to low levels of fluoride exposure (e.g. 1 mg per day)? These individuals report experiencing a variety of symptoms that are reversed when the source of fluoride is removed and reappear when the fluoride is introduced. Please note: The Australian National Health and Medical Research Council recommended such scientific studies be carried out in 1991 (NHMRC, 1991), but not one has been carried out in the 22 years since this recommendation was made. See more discussion on this topic in chapter 13 of our book and in Spittle (2008).
6) Can you find any attempt by any health agency in any fluoridated country to follow up the finding by Schlesinger et al, 1956 in the Newburg-Kingston, NY fluoridation trial, that the young girls in the fluoridated community were menstruating on average 5 months earlier than the young girls in the non-fluoridated community?
7) Repeating an earlier request discussed above, can you provide a list of animal and human studies that nullify the weight of evidence I have listed above that indicate that fluoride is a neurotoxicant with an inadequate margin of safety to protect all children (including those with nutrient deficiencies) drinking uncontrolled amounts of fluoridated water in addition to fluoride ingested from other sources?
8) Can you point to any studies conducted in fluoridated countries that have convinced you that exposing babies to fluoridated water causes no other damage to their developing tissues other than the damage to their growing tooth cells leading to dental fluorosis? Or is this just wishful thinking on the part of proponents? Is it likely that the fluoride ion would confine its biochemical interference only to the growing tooth cells? What about bone cells? Brain cells? Thyroid gland cells?
9) Can you find any study carried out in NZ or any other fluoridated country that has set out to assess total exposure to fluoride by monitoring fluoride levels in bones at either biopsy during operations or at autopsy? Note: this was another suggestion made by the Australian NHMRC in 1991 but was never pursued by any Australian health agency.
10) What studies carried out in NZ have investigated any health concerns in fluoridated communities? I couldn’t find many can you? Would you agree that the absence of study is not the same as absence of harm?
The evidence of fluoridation’s effectiveness is weak
Similarly, we need to tighten up the discussion of fluoridation’s effectiveness. A scientific proponent like Ken should be able to present the primary scientific studies and weight of evidence analysis that has convinced him that drinking fluoridated water leads to a significant reduction in tooth decay. Being able to offer a theoretical mechanism of action (and I discuss some of Ken’s ideas on this below) is only part of the requirement.
In chapters 6-8 of our book we present the case that the evidence that swallowing fluoride or drinking fluoridated water reduces tooth decay by a significant amount – is very weak – especially in the permanent teeth. This is especially apparent in the larger studies like the US National Institute of Dental Research (NIDR) study reported by Brunelle and Carlos in 1990 (this incidentally was the largest survey of tooth decay ever carried out in the US). The authors looked at 39,000 children in 84 communities and reported an average saving in tooth decay for 5 to 17-year-olds of just 0.6 of one permanent tooth surface (see Table 6). This meager saving of 0.6 of one tooth surface out of over 100 permanent tooth surfaces in a child’s mouth was not even shown by the authors to be statistically significant. I think for most people such a benefit – even if it was real – would be of an insufficient magnitude to justify forcing the practice on people or taking the many health risks involved, especially the possibility that we may be lowering the IQ of some of our children.
So where are the comparable studies that Ken has read that offset the Brunelle and Carlos study and the other studies and reviews that we cite in chapters 6-8 (Ziegelbecker, 1981, 1993; Leverett, 1982; Colquhoun, 1984, 1986,1987, 1990, 1992, 1995 and 1997; Diesendorf, 1986; Colquhoun and Mann, 1986; Gray, 1987; Yiamouyiannis, 1990; Steelink, 1992; Teotia and Teotia, 1994; Spencer et al., 1996; de Liefde, 1998; Kumar et al., 1998; Colquhoun and Wilson, 1999; Locker, 1999; McDonagh et al, 2000; Kumar et al., 2005; Komárek et al, 2005; Cheng et al., 2007; Pizzo et al., 2007; Osmunson, 2007 and Warren et al., 2009).
To these studies we must add in a weight of evidence approach two other facts: 1) several modern studies have not found tooth decay to increase when fluoridation has been stopped in various communities in Finland, former East Germany, Cuba and British Columbia, Canada and 2) the many press reports from major cities in the US of a dental crisis in low-income areas even though they have been fluoridated for over 20 years (for citations see Chapter 8 in The Case Against Fluoride…).
Again what we are looking for here is a presentation of the evidence by Ken that would persuade an independent observer that the weight of evidence for effectiveness is very strong and outweighs the evidence of little benefit presented in the studies cited above.
Ken’s topical mechanism via saliva and plaque
As with other proponents of fluoridation, Ken asserts that fluoridated water works topically, by increasing the level of fluoride in saliva and plaque. There is scarce data, however, to support this claim. Ken cites four papers (only one of which is a primary study), but as I discuss below, these papers do little to answer the key questions: namely: (1) are the saliva and plaque F levels produced by fluoridation high enough and of sufficient duration to prevent caries, and, if so, (2) are the differences in saliva and plaque F levels between children in fluoridated and non-fluoridated communities of sufficient magnitude to produce a meaningful difference in caries?
There is scarce data in the four papers Ken cites (Cury & Tenuta 2008, Martínez-Mier 2012; Featherstone 1999, Bruun & Thylstrup 1984). Of the papers, only Bruun & Thylstrup 1984 is an actual study, and it deals with a high-fluoride community (2.31 ppm), and thus, were it a study on adverse health effects, I suspect Ken might claim it irrelevant to fluoridation. But, assuming it is relevant, it’s worth noting that – although the authors found a lower caries rate in the high-F community (vs a community with 0.36 ppm) — the authors note that their “analyses relating the individual fluoride concentrations in whole saliva to the clinical caries scores within each of the two areas indicated that no causal relationships seem to exist between these two parameters.” So, while the authors conclude that “frequently increased availability of fluoride in the oral fluids due to [waterborne fluoride] has an important relationship to the reduced caries experience observed in the high F area,” their conclusion can be questioned, particularly as it relates to the 0.7 ppm water F level used in fluoridated communities.
So, what is the evidence that the saliva and plaque levels produced by fluoridated water exerts a significant topical benefit? According to the reviews that Ken cites (and the notably few studies that these reviews reference), the average saliva F level among children in a community with 1.2 ppm fluoride is 16.5 ppb with daily fluctuations that range as high as 144 ppb (Oliveby 1990, cited by Cury). To put these saliva levels in context, Featherstone states that 30 ppb is the lowest level at which fluoride has been observed to have an effect on tooth mineralization, with >80 ppb being the “optimum” (Featherstone 1999). Featherstone supports this statement by citing a single study – Brown (1977). Assuming that Brown’s study can be replicated, it is evident that the average saliva F level in a 1.2 ppm community — let alone a 0.7 ppm community — is not sufficient to affect tooth mineralization. Any topical effect of fluoridated water, therefore, must either come from the transient spikes in saliva F or the residual F in plaque. Judging by the papers Ken cites, the evidence supporting either of these scenarios is meager at best.
I’ll start first with the transient spikes in saliva F. While spikes in saliva F in fluoridated areas can exceed the levels (30 to 80 ppb) that Featherstone claims can affect teeth, this does not tell us a great deal. To be relevant, it must be shown that the transient spikes are not only high enough, but long enough, to have an effect. Neither Featherstone, nor any of the other papers cited by Ken provides data to answer this question. Further, even if the transient spikes are of sufficient duration to have an effect, it must be asked whether this effect is of any practical import in the current era when the vast majority of children in non-fluoridated areas brush their teeth with fluoride toothpaste? The importance of this latter question is obvious in light of Featherstone’s observation that “fluoride can be retained at concentrations in the saliva between 0.03 and 0.1 ppm for 2-6 hours” after the use of fluoridated dental products.
I’ll now turn to the question of plaque fluoride. Only one of the papers cited by Ken appears to provide any data on the difference in plaque F levels between fluoridated and non-fluoridated communities (Cury & Tenuta 2008). The plaque F data that Cury & Tenuta cite is not only unpublished, but is at rather stark odds with previously published data (See Whitford 2005). Cury & Tenuta claim “an almost 20-fold difference” in plaque F levels (3.2 ppm vs. 0.2 ppm). Whitford, however, found far higher F levels in the plaque (~50 to 450 ppm) and a far smaller difference (2-to-5 fold) between the fluoridated and non-fluoridated community. But Whitford’s study was itself quite peculiar as the unfluoridated community was in Brazil, but the fluoridated community was in the U.S. If children in the U.S. community had greater exposure to fluoride from other sources (which is not only possible, but likely), then the difference in plaque F levels is even smaller than Whitford’s study suggests.
In any event, whatever the difference in plaque F levels is, we should have ample data showing that this differential is sufficiently large to produce a significant and practical effect. I am unaware of any such study, so I will be quite curious to see how many Ken can cite. This shouldn’t, of course, be a difficult task: if plaque F is considered the main vehicle by which fluoridated water exerts a topical benefit, there should be no shortage of primary studies that Ken can cite demonstrating that the plaque F seen in fluoridated areas [x plaque F level] is far superior to the plaque F level seen in non-fluoridated areas [y plaque F level]. I look forward, therefore, to seeing the studies that Ken cites — particularly when considering that Buzalaf found that toothpastes containing 500 ppm fluoride are not effective at controlling caries (Buzalaf 2013). By way of reference 500 ppm is more than twice the background plaque F levels seen in fluoridated areas according to Whitford, 2005.
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