Do we need a new fluoride debate?

I think we do. Something like the good faith scientific exchange I had with Paul Connett four years ago (see Connett & Perrott, 2014 – The Fluoride Debate).

After all, there have been a number of important scientific reports since then. They may have been thrashed out (and thrash is sometimes the operative word) in one of the “anti-fluoride” or “pro-fluoride” internet silos but there has yet to be a proper discussion.

I have been trying to get one going for a while. Paul Connett is no longer interested and everyone else on the “anti-fluoride” side seems unwilling. However, Bill Osmunson who recently replaced Paul Connett as director of the Fluoride Action Network has been contributing to the discussion on several of the posts here. He seems to be the obvious choice for a discussion partner and I  asked him if he is willing to participate in another scientific exchange of the sort I had with Connett.

So far he has not responded – but as he has made some relevant critiques of several recent scientific papers in these discussion contributions I think it is relevant to bring that discussion into the formal blog posts. Otherwise, some important points will just be lost because they are buried deep in the discussion threads.

Here I respond to criticisms Bill makes of two recent studies which looked for evidence of the influence of community water fluoridation (CWF) on IQ and cognitive deficits in general. I urge Bill Osmunson to respond to my points in a format which can be presented as a blog post here.

Community water fluoridation and IQ

The two studies were published after my exchange with Paul Connett and are:

Broadbent, J. M., Thomson, W. M., Ramrakha, S., Moffitt, T. E., Zeng, J., Foster Page, L. A., & Poulton, R. (2014). Community Water Fluoridation and Intelligence: Prospective Study in New Zealand. American Journal of Public Health, 105(1), 72–76.

And

Barberio, A. M., Quiñonez, C., Hosein, F. S., & McLaren, L. (2017). Fluoride exposure and reported learning disability diagnosis among Canadian children: Implications for community water fluoridation. Can J Public Health, 108(3), 229.

Broadbent et al., (2014)

This study used data from the Dunedin  Multidisciplinary Health and Development longitudinal study and found no difference in IQ of people in fluoridated and unfluoridated areas or any effect of fluoridated toothpaste or fluoride supplement use.

I hope I represent Bill correctly but his criticisms of this study are vague – I can’t help feeling he is succumbing to the general hostility anti-fluoride campaigners have had about this study.

Let’s deal with his last criticism:

” I have previously presented my reservations about the NZ study and Broadbent’s comparing fluoridation with fluoride supplements, which lacked power to evaluate IQ.”

It more or less encapsulates anti-fluoride criticisms of the study and does contain an element of validity in reference to the study’s “power.” However, Bill’s reference to “power” is far too vague. It needs to be quantified.

Is Bill claiming that there are declines in IQ caused by CWF but they are too small to be detected in a study like Broadbent et al., (2014)? Or was there something about that study which made it incapable of detecting a reasonable IQ decline? Or does it matter – after all someone who is ideologically committed to believing fluoride is bad for IQ can always fall back on this argument when experimental results don’t go their way. No study will realistically have the ability to detect an extremely small IQ change that they might argue for. And such a small change is more in the eye of the (biased) observer than a reality.

Fellow FAN members Hirzy et al., (2016) also argued that the “power” of the Broadbent et al.,  (2014) study was too low to detect their assumed change in IQ. They argued this case on the basis of total dietary intake of fluoride claiming that there was very little difference of total dietary intake between fluoridated and fluoridated areas.  Osmunson et al., (2016) made the same argument – appearing to give up completely on the contribution of CWF (as it “likely represents less than 50% of total fluoride intake”) and directing attention to total fluoride intake instead. However, their arguments are very subjective as they pull dietary data “out of a hat” and don’t deal with the real situation where the study occurred.

Osmunson mentioned the importance of fluoride supplements and fluoride toothpaste to fluoride intake but seemed to have missed the fact that Broadbent et al., (2014) had also included these as factors in their statistical analysis. Neither these factors nor CWF exhibited a statistically significant effect on IQ.

The apparent fallback position of Hirzy et al., (2016) and Osmunson et al., (2016) that the relatively small dietary F intake meant their assumed IQ differences were too small for the study to detect comes across as straw-clutching. Especially as oral health differences between fluoridated and unfluoridated areas were detectable See Evans et al., 1980 and Evans et al., 1984).

The “power” of a study

The “element of validity” I referred to in Bill’s complaint about the “power” of the experiment is one every practical researcher faces – especially when dealing with an existing programme rather than designing, from the ground up, a laboratory experiment. Numbers of participants, or samples, are always limited and researchers rarely have the luxury of the large number they would wish for to provide more “power.”

The “power” of a study is often represented by the  95% confidence interval (CI). This means that if the same population is sampled on numerous occasions and interval estimates are made on each occasion, the resulting intervals would bracket the true  population parameter in approximately 95 % of the cases.” Usually, more sample numbers mean a smaller CI and therefore more confidence in the value of the result.

Broadbent et al (2014) reported a 95%CI of -3.22 to 3.20 IQ points for the effect of community water fluoridation with children of 7 -13 years. (The equivalent CIs for the effects of fluoride toothpaste and fluoride tablets were -1.03 to 2.43 and -0.38 to 3.49 respectively). The observed effects were not statistically different to zero. Their study used just 990 children. If more participants had been available the 95%CI could have been reduced to less than the range of 6.4 IQ points actually found for the effect of CWF.

In a very large Swedish study, Aggeborn & Öhman (2016) included between 20,000 and 80,000 participants and estimated a confidence interval of -0.23 to 0.89 IQ units when fluoride is increased by 1 mg/L. (They were able to consider a continuous measure of fluoride and not simply fluoridated or unfluoridated treatments). This study has far more “power” than that of Broadbent et al., (2014), and therefore a smaller CI value. But the conclusion was the same – fluoride at these concentrations had “a zero-effect on cognitive ability.”

Barberio et al., (2017)

This is a Canadian study with a large representative sample and individual estimates of fluoride exposure and reported learning disability diagnosis. Overall it concluded there was no “robust association between fluoride exposure and reported learning disability diagnosis.”

Bill Osmunson argues that this study “has limitations” and that the “conclusions overstate their data.”

I agree with Bill that diagnosis of learning disability based on a household questionnaire is not the same as a proper professional diagnosis, although presumably the question aimed at finding out if a professional diagnosis had been made – and what it was in some cases. The authors acknowledge that weakness but argue that more objective assessments are probably only feasible in small-scale studies.

Interestingly Bill and his fellow anti-fluoride campaigners did not raise this problem of reliance on parental answers to a questionnaire when they considered and argued strongly for, the Malin and Till (2015) ADHD study. (See  Perrott 2017 – Fluoridation and attention deficit hyperactivity disorder – a critique of Malin and Till (2015)for more details of this study and its problems.

Of course, these are the real-world problems faced by researchers attempting to extract useful data from large-scale surveys. One of the reasons why readers should not consider single studies as definitive and should consider each one critically and sensibly.

However, I think Bill is straw-clutching when he quotes the authors:

“When Cycles 2 and 3 were combined, a small but statistically significant effect was observed such that children with higher urinary fluoride had higher odds of having a reported learning disability in the adjusted model (p = 0.03).” [Cycles 1 and 2 are two separate parts – 2009-20011 and 2012-2013 respectively – of the Canadian Health Measures Survey]

And then argues:

“Barberio could have concluded they found harm. Instead, they focused on data which did not show harm.”

Bill is aware that a statistically significant effect of fluoride exposure was observed in only a limited case – when data from two cycles were combined and the urinary fluoride data had not been corrected by using either creatine concentration or specific gravity. This correction is necessary as an attempt to overcome the shortcomings of single spot-samples of urine. As the authors point out “spot urine samples used to measure fluoride are vulnerable to fluctuations.” And :

“creatinine-adjusted urinary fluoride or specific gravity-adjusted urinary fluoride . . .  are thought to be more accurate because they help to correct for the effect of urinary dilution, which can vary between individuals and different points in time. Accordingly, these adjusted measures help to offset some of the limitations associated with spot urine samples. The finding that the effect was reduced to non-significance when creatinine-adjusted and specific gravity-adjusted urinary fluoride were used, suggests that the association between urinary fluoride and reported learning disability diagnosis may not be robust.”

So Bill would prefer that the authors had based their conclusions on uncorrected urinary fluoride data and not the more reliable corrected figures? And why? Because that would have confirmed his bias. That is an unfortunate personal foible – our biases often encourage us to go with unreliable conclusions and not allow them to be challenged by the more reliable data.

Conclusions

Here I have simply considered the Broadbent et al., (2014) and Barberio et al.,. (2017) papers because these are the ones Bill Osmunson has responded to. I urge him, to also consider the Aggeborn and Öhman (2016) paper.

I hope Bill Osmunson will respond to this post with his refutations of my points or further arguments about these and other papers. I hope also that he takes up my offer of space here for an in-depth exchange of the sort I had with Paul Connett four years ago.

References

Aggeborn, L., & Öhman, M. (2016). The Effects of Fluoride In The Drinking Water.

Barberio, A. M., Quiñonez, C., Hosein, F. S., & McLaren, L. (2017). Fluoride exposure and reported learning disability diagnosis among Canadian children: Implications for community water fluoridation. Can J Public Health, 108(3), 229.

Broadbent, J. M., Thomson, W. M., Ramrakha, S., Moffitt, T. E., Zeng, J., Foster Page, L. A., & Poulton, R. (2014). Community Water Fluoridation and Intelligence: Prospective Study in New Zealand. American Journal of Public Health, 105(1), 72–76.

Evans, R. W., Beck, D. J., & Brown, R. H. (1980). Dental health of 5-year-old children: a report from the Dunedin Multidisciplinary Child Development Study. The New Zealand Dental Journal, 76(346), 179–86.

Evans, R. W., Beck, D. J., Brown, R. H., & Silva, P. A. (1984). Relationship between fluoridation and socioeconomic status on dental caries experience in 5-year-old New Zealand children. Community Dentistry and Oral Epidemiology, 12(1), 5–9.

Hirzy, J. W., Connett, P., Xiang, Q., Spittle, B. J., & Kennedy, D. C. (2016). Developmental neurotoxicity of fluoride: a quantitative risk analysis towards establishing a safe daily dose of fluoride for children. Fluoride, 49(December), 379–400.

Malin, A. J., & Till, C. (2015). Exposure to fluoridated water and attention deficit hyperactivity disorder prevalence among children and adolescents in the United States: an ecological association. Environmental Health, 14.

Osmunson, B., Limeback, H., & Neurath, C. (2016). Study incapable of detecting IQ loss from fluoride. American Journal of Public Health, 106(2), 212–2013.

Perrott, K. W. (20217). Fluoridation and attention deficit hyperactivity disorder – a critique of Malin and Till (2015)).  British Dental Journal, In press.

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8 responses to “Do we need a new fluoride debate?

  1. Bill Osmunson DDS, MPH Director, Fluoride Action Network

    Ken,
    I would be pleased to discuss fluoride and health.

    The topic has several streams of evidence.

    In order to make a “judgment,” we need to consider all streams of evidence, not just one. . . such as neurotoxicity, rather inclusive of all.

    A. What dosage of fluoride is beneficial . . if any?

    B. What is the range of fluoride exposure in the population without supplementation? What is the difference which should be supplemented?

    C. What government agency is charged with determining the dosage to achieve the benefit?

    D. What is the optimal tooth fluoride concentration which demonstrates a reduction in dental caries? And the serum fluoride concentration to achieve the optimal tooth fluoride concentration? And the optimal total exposure (dosage) of fluoride to achieve both the serum and tooth fluoride concentration?

    E. What quality of research will we accept as evidence of benefit?

    F. What margin of safety is acceptable?

    G. What percentage of the public harmed is acceptable?

    H. What is the measured evidence of cost savings?

    I. What are the potential risks from excess fluoride exposure and at what dosage and at what age?

    J. What are the synergistic effects of other chemicals and fluoride? For example, it appears there is a curve of “benefit” from fluoride as the concentration changes. Excess fluoride causes caries. And the caries rates change with a change in the calcium and magnesium rates in the water. If we are to adjust the chemicals in water to reduce dental caries, we need to also adjust fluoride based on calcium and magnesium concentrations.

    k. What are the genomic factors which create greater or lesser sensitivity to fluoride?

    After all, if there is little or no benefit, any potential risk or expense is unacceptable. If the benefit is significant, then greater risk to some should be considered.

    Perhaps terms should be clearly defined. For example, the term “endemic” is used for a disease or condition found “in people.” Often the term is used for communities with high fluoride exposures, water, coal, tea, etc. However, fluoride can be abundant in water, foods, air, soil, etc. When referring to water, virtually all water has some fluoride. Water fluoridation is the “adjustment” of existing or “endemic” fluoride concentration to achieve a water fluoride concentration, not an individual dosage of fluoride. Does the term “endemic” mean “found in people” or “found in the person” or “found in the community” or “found in the country?” Fluoride is found virtually everywhere. At what individual or range of dosage(s) is fluoride considered “endemic?”

    Probably more points to consider, but these are some of the streams of evidence for discussion.

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  2. Thanks for agreeing to an online discussion, Bill. If you send me your response to this post, including any new arguments you wish to make, I will put it up as a separate post. Of course, I will not make any changes except for those required by formatting. I have emailed you about this.

    Look forward to a fruitful exchange of views and a good scientific discussion of the issue.

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  3. Bill Osmunson DDS, MPH

    Ken,
    When “lovers” quarrel, part of the problem is their understanding of words and another is their intent to misunderstand, defensive. If your intent is to weigh the evidence, I am willing to spend my time with you. If your intent is to pick at the flaws of each study with bias, then we are not having a debate but an argument and fight. Not interested.

    The overriding principle is, “the person/people manufacturing the substance have the obligation to prove their claims of safety and efficacy are true.”

    You encourage governments to give each person additional fluoride without their consent, because you imply fluoride at dosages consumed by the public is “safe and effective.” It is your job to prove efficacy and safety with a label with the evidence from the manufacturer.

    It is not my job to provide you with the research on “safety and efficacy” at dosages ingested by the public. That is your job.

    What is the range of dosages ingested by the public with and without the addition of fluoride to water? Please answer. Serum, urine, total exposure?

    How much are we ingesting is the first logical question and you have failed to answer.

    Then we need to determine how much fluoride is desired to reduce dental caries? What is the optimal tooth fluoride concentration? Please answer.

    Then determine the amount which is safe.

    Those are fundamental questions of pharmacology. Please answer with measured evidence. Preferably provide primary references from the final manufacturer, water supplier.

    There are weakness on both sides of the fluoridation debate. If you are unwilling to consider the weakness of both sides, then you have blind religious fervor and debate is a waste of time.

    How much are we getting? How much is optimal for the tooth, the target organ? How much is safe? Measured evidence please.

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  4. Bill Osmunson DDS, MPH

    Ken,
    You asked me to comment on Aggeborn & Öhman (2016). The link you provided is not a peer reviewed published study, apparently a thesis by two economic students.

    I’m not trying to say the study has no value, but it has some serious weaknesses.

    I do not appreciate you starting your rant above with labels and gossip, hardly professional. If you want to debate the science, fine. If you want to put value judgments on people, then I’m not interested.

    Remember, I promoted fluoridation for about 25 years. Objective evaluation of all the streams of evidence provided me with only one ethical conclusion, stop fluoridation. No one study is proof.

    And early on, you say, ” Bill’s reference to “power” is far too vague. It needs to be quantified.” You know exactly what I was talking about, because you go into details later. Again, you are attempting to show how “smart” you are, rather than understand what I am saying. Reminds me of my President. I expected you, a scientist, to understand “power.”

    I understand what you are saying. You find Broadbent to have validity and evidence of safety. I disagree, because Broadbent predominantly compared the effects of fluoridated water with fluoride supplements. Broadbent and you have glossed over fluoride supplements. Without measured fluoride exposure in either urine, serum, or tooth, Broadbent was estimating and speculating on total exposure and comparing two exposure methods of delivery rather than water fluoridation.

    I don’t know how much weight you put on the Broadbent study, but as a public health clinician, most of the subjects had fluoride from one of two sources. Total fluoride exposure was not adequately considered. Broadbent’s claims and conclusions are not supported by the data.

    After 70 years of fluoridation and these are the best studies promoters can come up with to demonstrate the neurotoxicological safety of fluoride? Give me a break. . . . Seriously inadequate. And a thesis by two economic students, not published or peer reviewed is interesting but caries little weight. Indeed, some aspects of the study were good, but total fluoride exposure including fluoride supplements was weak.

    Please provide the neurotoxicological safety studies at the dosage to achieve the tooth fluoride concentration which reduces dental caries.

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  5. Bill, you have undertaken to respond to my article with one of your own posted as an equal. Hopefully, in this, you will be specific. It is not an argument to point out that Aggeborn & Öhman (2016) is pre-publication and to say it has “serious weaknesses.” Any discussion will have to provide specific examples of your suggested weaknesses.

    I have no idea what you mean by “rant,” “labels” and “gossip.” My article surely is an attempt to deal with the science and your response, which I look forward to, should also do that.

    And, come on. It is not credible of you to cast my scientific analyses aside by accusing me of “being smart.” That is childish.

    Far from glossing over supplements Broadbent et al actually provided you with a confidence interval to enable you to judge to what extent they have any influence on IQ in this data. You should deal with that. You may be quite justified to claim this confidence level is large enough to hide the IQ effect (that is after all the purpose of the statistical analysis) but then, of course, you put yourself in the position of straw-grasping – trying to assert there is a very small effect without any evidence at all.

    Anyway, I do look forward to your article which will be the next post here and I will engage with that. It is best that detailed discussions be in these articles rather than in the comments sections.

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  6. Bill,

    You say “It is not my job to provide you with the research on “safety and efficacy” at dosages ingested by the public. That is your job.”

    However, since you claim that optimally fluoridated water supplies cause multiple problems in the populations drinking those water supplies, it becomes your job to provide evidence from those populations to support your claims.

    This does not mean that you reproduce 19th century textbook knowledge that areas with endemic fluorosis have problems, since we already know that.

    It means that you look at populations with optimally fluoridated water supplies and document problems in those populations (such as IQ, learning disabilities, etc).

    Now, millions of people worldwide have been drinking optimally fluoridated water supplies for seven decades. Those populations have been monitored for all that time, and data is available for them about teeth, employment, earnings, taxes, education, exam results, car ownership, house ownership, mental health, somatic health… The list goes on and on.

    Somewhere in all that monitoring is the data that you require to support or rebuff your so far evidence-free hypotheses about optimally fluoridated water supplies causing harm.

    How about supplying some evidence to support your claims rather than just saying “it is not my job”?

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  7. Bill, I do have some vague and very distant memories of “lovers quarrels.” But, gladly, those hormones no longer seem to be rushing through my system as the did in the old days. 🙂

    I hope we can treat each other with respect but I do not in any way want anyone to draw the conclusion that we are “lovers” from this.

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  8. Pingback: New fluoride debate falters – The Science Page

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