Tag Archives: fluoride

Flaw and porkie in anti-fluoride report claiming a flaw in Canadian study

Anti-fluoride group, Fluoride Action Network, ironically stamps their own critique of the Calgary fluoridation cessation study as “debunked.”

Anti-fluoride campaigners have launched another attack on a Canadian fluoridation cessation study. They claim it is flawed – but there is a huge flaw in their own critique.

I discussed their original attack in February last year (see Anti-fluoridationist’s flawed attacks on Calgary study). But this new attack is based on a published critique of the original study. I think that is good progress – the anti-fluoride campaigners have made a detailed critique and published it in the journal which published the original paper. The original authors have then responded. This is how things should be done.

Timeline

For those of you with the interest and time who want to go into the details, the original study was published in:

McLaren L, Patterson S, Thawer S, Faris P, McNeil D, Potestio M, Shwart L. (2016) Measuring the short-term impact of fluoridation cessation on dental caries in Grade 2 children using tooth surface indices. Community Dent Oral Epidemiol 2016.

The anti-fluoride critique was recently published in:

Neurath, C., Beck, J. S., Limeback, H., Sprules, W. G., Connett, M., Osmunson, B., & Davis, D. R. (2017). Limitations of fluoridation effectiveness studies: Lessons from Alberta, Canada. Community Dentistry and Oral Epidemiology, (October 2016), 1–7.

The response from the original authors was then published in:

McLaren, L., Patterson, S., Thawer, S., Faris, P., McNeil, D., & Potestio, M. (2017). Fluoridation cessation: More science from Alberta. Community Dentistry and Oral Epidemiology, (October), 1–3.

Other data which have been used in the critique and which I will use here can be found in:

McLaren, L., McNeil, D. A., Potestio, M., Patterson, S., Thawer, S., Faris, P., … Shwart, L. (2016). Equity in children’s dental caries before and after cessation of community water fluoridation: differential impact by dental insurance status and geographic material deprivation. International Journal for Equity in Health, 15(1), 24.

And:

McLaren, L., Patterson, S., Thawer, S., Faris, P., McNeil, D., Potestioa, M. L., & Shwart. L. (2017). Exploring the short-term impact of community water fluoridation cessation on children’s dental caries: a natural experiment in Alberta, Canada. Public Health, 146, 56–64.

Most of the authors of the critique are listed as members of the Fluoride Action Network (FAN) team and I can understand that FAN would feel proud that their critique was published. However, I feel their press release was rather underhand to imply the original study is:

“seriously flawed science  . . . Citizens should be concerned that their tax dollars have funded this biased work.”

And that the work was funded by state and public bodies:

“whose policy is to promote fluoridation.”

But let’s look at the critique itself – because it has some pretty big flaws itself.

What did the original study find?

My article, Anti-fluoridationist’s flawed attacks on Calgary study describes the details of this study. But briefly, it showed that child tooth decay increased in the Canadian city of Calgary after cessation of fluoridation. It used a comparison fluoridated city (the nearby and similar sized city of Edmonton) – and just as well because tooth decay also increased in that city during that time. However, there was still an increase in tooth decay in Calgary after cessation of fluoridation even after correction for the increase due to other factors apparent in Edmonton.

What did the critique claim?

A number of the criticisms are debatable and relatively minor.

How suitable was Edmonton as a comparison city? Neurath et al., (2017) claim it wasn’t suitable (but did not suggest a better alternative). McLaren et al., (2017) claim there is “no better comparison community for Calgary than Edmonton.”

Confounding – Neurath claims consideration of confounding factors was inadequate. McLaren et al., (2017) refer to extra data in two other papers and describes their consideration of several likely confounding factors like public health programmes and use of sealants. Whether the correct factors or sufficient factors were considered is always a bone of contention between authors and critics and, in the end, available data and funding decides.

Study design – Neurath et al., (2017) argue for randomised controlled trials. McLaren et al. (2017) point out that in studies of social programmes one must go with what exists. They say:

“While we agree with the value of stronger designs, one must be thoughtful about evaluation of public health measures, which by definition are complex and context-dependent. We used the best available
data and design for our circumstances”

Data ignored?

But Neurath et al (2017)’s major criticism is that some important data was ignored. And they claim that when that data is included the conclusions are not valid.

Of course, the FAN authors are stretching things quite a bit. The original study was based on data for tooth surfaces – the decay, extracted and filled tooth surfaces (defs). This was used as it is more sensitive than the tooth data itself – the decayed missing and filled teeth (deft).

Data for defs were only available for the 2004/05 and 2014/15 surveys. Unfortunately, there were no defs data for the pre-cessation period closer to the time of cessation (2011). That is the sort of problem researchers face when dealing with existing surveys and existing social programmes.

But the bright sparks at FAN latched on to the fact there was a survey with deft data in Calgary closer to the cessation time – 2009/2010. The fact that there was no equivalent survey for Edmonton didn’t hold them back – they proceeded to imply the 2009/2010 data had been purposely held back, despite McLaren making clear she could not use that data for Calgary in the absence of similar data for Edmonton. That would have negated the requirement for a comparison city and the existing data surely shows that requirement was very wise.

So Neurath et al., (2017) chose to ignore the obvious requirement for a comparison city and proceeded to argue their case on the Calgary data alone. They argued the study was “fatally flawed” and that “key data [was] omitted.” The argument implied the study was somehow fraudulent and that the authors had hidden the 2009/2010 survey data – despite the fact this data is used in another of their papers!

Neurath et al., (2017) pretend that a comparison city is not really necessary – relying only on the tooth data (deft) for Calgary they argue that as 50% of the increased in tooth decay had occurred between the 2004/05 and 2009/10 surveys then the increases seen after cessation of fluoridation was due to the same trend (see their Figure 1 below). They argued this proved that cessation of fluoridation had no effect. Ignoring completely the Edmonton data.

So, an obvious flaw in their critique – but wait, there is more! They actually go so far as to falsify data.

Falsifying a “correction factor”

Not satisfied with the plots in Figure 1B they found a way to make the data look even worse for McLaren et al. (2015). They came up with a “correction” factor to convert the deft data for 2009/2010 survey into defs data. Here is their Figure 2 using the “converted” deft data

Looks bad, doesn’t it?

However, the trick is in the way the conversion factor is calculated. They “used the ratio of defs to deft in the 2013/2014 survey to make the conversion.” The table below for subset (dmft>0) data they used shows this produces a conversion factor of 2.41 – big enough to dramatically push the 2009/10 data point right up so that it is sitting on the Edmonton “trend line” in their Figure 2 above.

But they could have equally used the ratio of defs/deft in the 2004/2005 survey to make the conversion. That produces a much lower conversion factor of 1.63 – which is not at all consistent with their claim “when we applied this conversion [2.41] to the 2004/2005 Calgary survey, where both deft and defs are known, the calculated defs was very close to the known defs.”

In fact, it may have been more appropriate to take the average conversion factors from the two available surveys. In the figure below I have done this (green data point) and compared this with the use of the conversion factors from the 2004/05 survey (purple data point) and that from the 2004/15 survey used by Neurath et al (yellow data point).

I guess this shows the danger of making these sort of adjustments – especially when there is a bias to confirm. And also that readers should beware of vague assertions of the sort:

“when we applied this conversion [2.41] to the 2004/2005 Calgary survey, where both deft and defs are known, the calculated defs was very close to the known defs.”

Conclusion

The McLaren et al., (2017) study has its limitations, limitations admitted and described by the authors. But, it is the FAN critique of Neurath et al., (2017) rather than the original study, that is fatally flawed. Flawed because of confirmation bias and a porky.

1: They ignored the necessary use of a comparison city and assumed the increase in tooth decay in Calgary was linear over the time between the two surveys McLaren at al used.

2: The use of any correction factor would be questionable but Neurath et al., (20127) clearly used a biased value to suit their argument. Further, they purposely misrepresented their correction factor by implying a similar value would have been obtained from the 2004/2005 survey data. Completely wrong.

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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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Endemic fluorosis and its health effects

Much of the anti-fluoridation propaganda used by activists rely on studies done in areas of endemic fluorosis. Slide from a presentation by Q. Xiang to an anti-fluoride meeting organised by Paul Connett’s Fluoride Action Network in 2014.

 

The public debate in New Zealand might convince the casual reader that all the science related to fluoride revolves around tooth decay and IQ. But that is certainly not the case on a world scale.

The World Health Organisation gives guidelines for the concentration of fluoride in drinking water recommending it should be in the range 0.5 – 1.5 mg/L. OK, above 0.5 mg/L because of the positive effect it has on oral health, in reducing dental decay. That interests us in New Zealand because our drinking water is more likely to be deficient in fluoride.

But on the world scale, many people are far more interest in the higher limit – or at least in attempting to reduce their drinking water fluoride concentration to below this limit. This is because large areas of the world suffer from the health effects of endemic fluorosis due to the excessive dietary intake of fluoride and the high concentration in their drinking water.

There are significant health effects from endemic fluorosis – effects we don’t’ have here but are important to many countries. So there is plenty of research – both on the health effects and on reducing drinking water concentrations and dietary intake.

In fact, the anti-fluoride campaigners get all the scientific reports they use in “evidence” to oppose community water fluoridation from studies in countries where fluorosis is endemic. Not only is this misrepresenting the science. It is also unbalanced because scientific studies on IQ in areas of endemic fluorosis represent only a small proportion of such health-related studies.

To illustrate this I have done a number of searches on Google Scholar using the terms “endemic fluorosis” and one other term related to a health effect. Here is the resulting table.

“endemic fluorosis” and “?” Hits in Google Scholar
Alone 8810
And “dental fluorosis” 3570
And “bone” 3570
And “skeletal fluorosis” 2910
And “cancer” 1690
And “death” 1180
And “birth” 1170
And “osteoporosis” 1130
And “body weight” 936
And “gastrointestinal” 808
And “Osteoclerosis 697
And “diabetes” 642
And “cardiovascular” 633
And “reproduction” 592
And “IQ” 480
And “cognitive” 331
And “heart disease” 327
And “hypothyroidism” 297
And “Renal failure” 292
And “obesity” 230
And “infertility” 216
And “non-skeletal fluorosis” 183
And “muscoskeletal” 178
And “birth weight” 135
And “birth defects” 86
And “premature birth” 29

40% of the hits related to “dental fluorosis” and another 40% to “bone” while 33% related to “skeletal “fluorosis.” Obviously, these are of big concern in areas of endemic fluorosis so receive a lot of research attention. In fact, the prevalence of these is used to define an area as endemic.

But only 5% of hits related to IQ – clearly of much less concern to researchers. Yet it seems to be all we hear about here and this illustrates how unbalanced most of the media reports we get here are.

To start with, these health effects do not occur in countries like New Zealand using community water fluoridation. They occur in regions where drinking water contains excessive fluoride and where the dietary intake of fluoride is excessive.

But the other fact is that IQ effects receive relatively little attention in health studies from those areas compared with the more obvious, and more crippling, effects like dental and skeletal fluorosis.

Mind you, that doesn’t stop activists making sporadic claims of all sorts of health effects from fluoridation and relying on studies from areas of endemic fluorosis. But the most frequent claims made by activists at the moment relate to IQ. Perhaps this is because it is harder to hide the fact that we don’t see cases fo skeletal fluorosis or severe dental fluorosis in New Zealand. IQ changes are not so obvious and this might make them a more useful tool for anti-fluoride campaigners to use in their scaremongering.

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Maternal urinary fluoride/IQ study – an update

Model of a fetus in the womb. Photo credit: CP PHOTO/ Alliance Atlantis/ HO) 

The maternal urinary fluoride/IQ study  (Bashash et al., 2017) continues to get attention – but mainly from anti-fluoride organisations. The scientific community will evaluate the published report after giving it due consideration and there have already been criticisms. But anti-fluoride campaigners consider it the best thing since sliced bread. The Fluoride Action Network (FAN) describes it as “a cannon shot across the bow of the 80 year old practice of artificial fluoridation” and Fluoride Free NZ insist that it “must spell an end to fluoridation in New Zealand.”

We expect confirmation bias from the anti-fluoride organisations. But the misrepresentations in the propaganda from these organisations are of more concern because they are blatantly meant to scaremonger.

Misrepresentation by anti-fluoride organisations

These people have worked hard to stress the respectability of the authors of the Bashash et al., (2017) paper and claim the study is impeccable. They are not interested in a critical analysis of the data and the conclusions. And they are completely silent about the evidence from the study showing no association of children’s urinary fluoride levels and IQ – normally they are quick to criticise authors reporting such a lack of association.

But this time as well as their normal misrepresentations they have actually manipulated a figure from the paper. I wonder what copyright law would say about this.

I provided the relevant figures from the paper my earlier article (see   Fluoride, pregnancy and the IQ of offspring) and commented on the large amount of scatter in the data.  This scatter should be a warning to any sensible reader – so FAN simply overcomes that problem by deleting the data points in their presentation of the figure.

Here is the original Figure 2 and the FAN misrepresentation of it:

Notice 2 things:

  1. The original figure showed the data for GCI – general cognitive index. It is not IQ and not presented as IQ in the original paper. But it is a measure  of “verbal, perceptual performance, quantitative, memory, and motor abilities of preschool-aged children.” Perhaps a fine point and FAN may be excused for inserting the more popularly understood term IQ. Or perhaps they decided not to use the real figure for IQ (Figure 3A) because it implied no effect at normal urinary fluoride levels (see figure 3A in Fluoride, pregnancy and the IQ of offspring);
  2. FAN removed all the data points in their presentation of the figure. I am sure FAN would argue this was to “simplify” the figure. But in doing so they have removed what is the most important information in Figure 2 – the wide scatter of the data points. That scatter suggests that even though the reported association is “statistically significant” it explains very little of the observed variation and is therefore not important (and may not even be real).

Association of maternal urinary F with child IQ poor and probably misleading

In Fluoride, pregnancy and the IQ of offspring I estimated that “the reported relationships with maternal urinary fluoride could explain no more than a few percent of the variation in the data.” Purely an estimation because I did not have the data to analyse myself and the authors did not give the relevant statistical information.

I have since used a plot digitiser programme to extract the data for these figures and performed my own statistical analysis.

These are the results:

For Figure 2:

Yes, a “statistically significant” relationship (p = 0.002) but it explains only 3.3% of the variation in GCI (R-squared = 0.033)

For Figure 3A:

Again, “statistically significant” (p = 0.006) but explaining only 3.6% of the variation in IQ (R-squared = 0.0357).

So my estimate was pretty good. And my evaluation is valid:

“In this case, I would expect that other risk-modifying factors that explain the variation more completely could be found. And if these were included in the multiple regressions there may not be any observable relationship with urinary fluoride.”

Considering that this work was unable to explain about 97% of the variation in CGI and IQ I really question its publication. Certainly, scientific evaluations will conclude that this paper should not have any influence on policymakers.

It’s a pity that with all the data the authors had they did not seek out, or properly evaluate, other possible risk-modifying factors.

Other work by group showing no association ignored

Strangely, the Bashash et al., (2017) paper did not include relevant IQ information from the PhD thesis of one of their team Deena B. Thomas. This is her thesis citation:

Thomas, D. B. (2014). Fluoride exposure during pregnancy and its effects on childhood neurobehavior: a study among mother-child pairs from Mexico City, Mexico. PhD thesis, University of Michigan.

It can be downloaded from the full-text link.

The data in chapter 2 of this thesis – Urinary and Plasma Fluoride Levels During Pregnancy and Determinants of Exposure Among Pregnant Women from Mexico City, Mexico – was published. The citation is:

Thomas, D. B., Basu, N., Martinez-Mier, E. A., Sánchez, B. N., Zhang, Z., Liu, Y., … Téllez-Rojo, M. M. (2016). Urinary and plasma fluoride levels in pregnant women from Mexico City. Environmental Research, 150, 489–495.

Bashash et al., (2017) did reference this paper – after all, it dealt with the data they used for estimating fluoride exposure. But they did not reference the thesis itself – and two other chapters in that thesis are directly relevant to the relationship of fluoride exposure to child IQ.

Chapter 3 – Prenatal fluoride exposure and neurobehavior: a prospective study – is directly relevant except that where Bashash et al., (2017) reported data for the children when 4 years old and 6-12 years old Thomas reported data for child neurobehavioral outcomes at ages 1, 2 and 3.

She concluded:

“that maternal intake of fluoride during pregnancy does not have a strong impact on offspring cognitive development in the first three years of life.”

OK – perhaps the difference is purely due to age. But surely it is part of the picture and should at least been mention in the Bashash et al., (2017) discussion.

Chapter 4 – Concurrent Fluoride and Total WASI in 6-15 year old children from Mexico City, Mexico – is also directly relevant because Bashash et al., (2017) did include that data in their paper. They concluded that:

“there was not a clear, statistically significant association between contemporaneous children’s urinary fluoride (CUFsg) and IQ either unadjusted
or adjusting for MUFcr.”

This differs a little from the findings in Thomas’s thesis:

“In the overall population, urinary fluoride appears to have no significant impact on total WASI scores (β =1.32, p=0.33), but this association changes once the models are separated by male and female children. Male children showed a significantly positive trend (β=3.81, p=0.05), and females showing a negative trend that was not significant (β= -1.57, p=0.39).” [WASI score is a measure of IQ]

And she wrote:

“analysis suggests concurrent urinary fluoride exposure has a strong positive impact on cognitive development among males aged 6-15 years.”

She concludes:

“These results were surprising in that they show opposite trends to what has been reported in the literature so, more studies with similar reliable methodology, which account for plasma fluoride, diurnal variations in urinary fluoride and children’s SES, are needed. If these results are substantiated, different fluoride interventions may be needed for male children versus female
children.”

I would have thought these findings and conclusions were worthy of discussion by Bashash et al., (2017). It’s not as if the authors were unaware of their colleague’s findings.

Maybe internal politics are involved. but that does not justify the omission.

Conclusion

The anti-fluoride people, and particularly FAN, are misrepresenting the study and have manipulated a figure to hide information in an unethical way. The data presented in the Bashash et al., (2017) study shows maternal urinary fluoride can only explain 3 – 4 % of the variation in General Cognitive Index and IQ of the children. The inclusion of a more viable risk-modifying factor would probably remove even that small amount explanation.  Bashash et al., (2017) also neglected to discuss relevant information from a colleague which contradicted their conclusions.

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Fluoride, pregnancy and the IQ of offspring

Anti-fluoride campaigners don’t agree. Image credit:Dental Care Tips for Mom and Baby” presentation

What’s the story about this new IQ-fluoride study? The one that claims fluoride intake by pregnant women could endanger their children’s IQ?

Whatever the truth, it has certainly got the anti-fluoride activists going. Mary O’Brien Byrne, leader of the local anti-fluoride group is even suggesting people check if their mothers lived in fluoridated areas. And they are busy promoting the newspaper articles on this. For example Fluoride exposure in utero linked to lower IQ in kids, study saysChildren’s IQ could be lowered by mothers drinking tap water while pregnant, and Higher levels of fluoride in urine linked to lower IQ scores in children.

Best not rely on those media reports, though – you know how unreliable they can be. The original paper is available – this is the citation:

Bashash, M., Thomas, D., Hu, H., Martinez-mier, E. A., Sanchez, B. N., Basu, N., … Hernández-avila, M. (2016). Prenatal Fluoride Exposure and Cognitive Outcomes in Children at 4 and 6 – 12 Years of Age in Mexico. Environmental Health Perspectives, 1, 1–12.

And here is a link to the full text. Download it and see what sense you make of it. I warn you it is a difficult paper to read.  A lot of information is lacking and the information that is included is hard to find. The statistical analysis is incomplete.

A new twist on the tired old fluoride/IQ story

Basically, it is the old drinking water fluoride causes lowering of IQ story. This time it relates to a supposed association of fluoride intake by pregnant mothers with cognitive deficits in their children. Interesting, only one other similar study (involving fluoride exposure while pregnant) has been reported – in January this year, and also in Mexico. I wrote about that study of Valdez Jiménez et al., (2017), In utero exposure to fluoride and cognitive development delay in infants,  in the article Premature births a factor in cognitive deficits observed in areas of endemic fluorosis?

Briefly, the Valdez Jiménez et al., (2017) study was from Mexican areas of endemic fluorosis with very high fluoride concentrations in drinking water so the results are not applicable to areas where community water fluoridation is used. However, the high incidence of premature births, and low birthweights for the children, for mothers with high urinary fluoride levels does suggest that problems of birth in areas of endemic fluorosis could provide a biological mechanism to explain the IQ deficits. Rather than a direct chemical toxicity mechanism.

What about the Bashash, et al. (2017) paper?

Generally, the paper concludes that “higher prenatal fluoride exposure . . . .was associated with lower scores on tests of cognitive function in the offspring.”

So here are some concerns I have about the paper

1: An association is not evidence of, or proof for, causation. Yes, that is the normal and obvious qualification for such studies and authors tend to repeat it – even if they might still attempt to argue the case that it is evidence. A lot of confirmation bias goes on with these sort of correlational studies.

2: The information about the mothers is scant. My first question, given it was Mexico, was did they come from areas of endemic fluorosis? The women were recruited from three hospitals in Mexico city but this says nothing about their current or former residential areas. No information on drinking water fluoride is presented nor any biological assessment, such as dental fluorosis, given which could help estimate the role of endemic fluorosis.

3: Assessment of fluoride exposure relied completely on urine fluoride concentration measurements. With between one and three samples for each mother-child pair! (Of the total sampled there was only one sample for 217, two for 224 and three for 71 mothers). I believe that is completely inadequate for estimating exposure – especially as fluoride levels in urine vary markedly during the day and with diet. Besides the extremely low sample numbers,  the World Health Organisation has warned that while urinary fluoride can be useful for monitoring populations “Urinary fluoride excretion is not suitable for predicting fluoride intake for individuals.”  (see Contemporary biological markers of exposure to fluoride). They further warn that 24 hr collection is preferred to the spot sampling used in this study.

4: The statistical information presented is confusing – and insufficient to estimate how relevant the reported statistically significant associations are. I believe the best idea of the data can be gleaned from the following figures presented in the paper.

Figure 2 displays the data and association of maternal urinary fluoride (MUFcr) with a general cognitive index (CGI) for the 4 yr old offspring.

Figure 3A displays the data and association of maternal urinary fluoride (MUFcr) with IQ of the offspring at age 6 -12.

While linear regression analysis showed statistically significant associations of the CGI and IQ of offspring’s with maternal urinary fluoride levels the large scatter indicates these associations will explain only a small part of the variations observed. In such situations, reliance on p values can be misleading. As a reader, I would be more interested in the R2 values which indicate the amount of variation explained by the association.

I estimate the reported relationships with maternal urinary fluoride could explain no more than a few percent of the variation in the data. In this case, I would expect that other risk-modifying factors that explain the variation more completely could be found. And if these were included in the multiple regressions there may not be any observable relationship with urinary fluoride.

I discussed this issue more fully in my article Fluoridation not associated with ADHD – a myth put to rest which showed that a published relationship of ADHD with fluoridation extent disappeared completely when altitude was included as a risk-modifying factor. And that relationship showed less scatter of the data points than in the figures above.

5: The absence of any association of child IQ to child urine fluoride was also reported in this paper. This conflicts with other researchers working in areas of endemic fluorosis who have reported such associations. It could be that the urine fluoride measurements used in the present study were not suitable. But I am picking that the anti-fluoride campaigners will be very silent about that information, given the importance they give to other studies showing a relationship in their propaganda.

Conclusions

it is a very unsatisfying paper. I couldn’t determine if areas of endemic fluorosis were implicated – as they were for the Valdez Jiménez et al., (2017) study. Urinary fluoride is an inadequate measure of fluoride exposure – especially for individuals and spot samples – and its variability does not allow comparison with other studies and other regions. I couldn’t evaluate if the reported results were relevant to New Zealand which does not have any endemic fluorosis.

Finally, I believe aspects of the statistical analysis were inadequate. But on the positive side, I am pleased the authors did display the actual data in their figures. The information in those figures forced me to conclude that maternal urinary fluoride may not have the influence the authors suggest. If it does have an influence its contribution can only be minor and other more important risk-modifying factors will be involved.

Mind you – I am sure anti-fluoride campaigners will see it differently. They are currently heavily promoting the study and anti-fluoride guru Paul Connett sees it as the best thing since sliced bread. He has gone on record to say this means the end of community water fluoridation!

Update

I think the anti-fluoride people are aware of weaknesses in this study. The local Fluyodie Free NZ has put out a press release including a figure which they have doctored to remove the data points which show how little variation is explained. Compare their figure with the Fiugure 2 above.

Fluoride Free NZ doctors figure from paper to hide the scatter in data points showing how little of the variability the relationship explains

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Facts about fluorosis – not a worry in New Zealand

This sort of serious dental fluorosis does not occur in New Zealand

A recent issue of the Fluoride Exposed Newsletter gives us the facts about dental fluorosis – a subject very often misrepresented by opponents of community water fluoridation.

Fluoride Exposed also explores what U.S. Surgeon Generals have done to promote prevention of both tooth decay and fluorosis in an article on their website, Is fluoride good for your teeth?:


Ever notice how words ending with “-osis” sound a bit scary?  That’s because “-osis” is a suffix (from the Greek) commonly used to describe disorders or abnormal states. Tuberculosis, multiple sclerosis…no fun. Those are serious.

Dental fluorosis is one of those things that sounds scarier than it actually is… at least if you live in a country like the good old U.S. of A., where public health and environmental protection agencies and organizations have made the scary kind of dental fluorosis (severe dental fluorosis) exceedingly rare.

Dental fluorosis is a little like blood pressure.  When it’s low, you’re good – in fact, mild dental fluorosis can protect your teeth from cavities.  Moderate dental fluorosis describes the appearance of tooth enamel when kids get exposed to a bit too much fluoride.  Changes range from barely visible white spots or streaks (in most cases) to white spots that are a cosmetic concern.  Severe forms involve staining and pitting.  These severe forms of fluorosis are super rare in the U.S. – because we have those protections we mentioned. In the States, we make sure fluoride isn’t too low or too high in drinking water.  It’s only in regions such as rural India, China, and the African Rift Valley, where severe dental fluorosis commonly reaches an actual disease state and affects tooth health and function.  But in the U.S., fluorosis is one of those things that’s not as scary as it sounds.

As you may already know, fluoride gets into your tooth enamel during the remineralization process and forms a super compound called fluoroapatite that resists decay.  For this reason, our dentists want us to get fluoride, ideally through drinking water and fluoride toothpaste.  Or if you’re in a community without fluoridated water, there are dental treatments and dietary supplements you can get.

But if a child who’s still developing teeth gets too much fluoride, dental fluorosis can occur while the teeth are still forming under the gums.  Data from the National Health and Nutrition Examination Survey (1999-2004) tells us that less than one-quarter of persons aged 6-49 in the United States had some form of dental fluorosis.

They even made a chart that shows the severity level of those affected:

Note: One interesting factoid: In this study, the rate of fluorosis for teenagers aged 12-15 was forty percent! That’s significantly higher than the rate for all age groups taken together.  It’s a data point we’ll be keeping an eye on in future studies.

According to the American Dental Association (ADA), the mild and moderate forms of dental fluorosis we have in the U.S. do not negatively affect the health of your teeth. It’s actually even correlated with some good things.  For example, rates of dental fluorosis are higher in kids whose teeth are more resistant to tooth decay.  Makes sense, right?

That said, we can make sure a child’s amount of fluoride is “just right” – enough to provide cavity protection, but not enough to cause visible changes in the tooth enamel.
5 ways to prevent kiddos from ingesting too much fluoride:

    1. Don’t give kids fluoride supplements if your drinking water is already at or above the recommended fluoride concentration of 0.7 mg/L.  You can find out if your water system fluoridates and at what level from this cool site from the CDC: https://nccd.cdc.gov/DOH_MWF/Default/Default.aspx.  Or call your water utility provider.
    2. If your drinking water contains greater than 2 mg/L of fluoride, children 8 years and younger should use an alternative source of drinking water.  A little less than 1% of Americans on public water systems have fluoride above this level.
    3. If you have well water, have it tested for fluoride levels, and again, use an alternative source for kids if fluoride is more than 2 mg/L.  Use an alternative source for everyone in the family if it tests at or above 4 mg/L.
    4. Use only a rice-grain-sized amount of fluoride toothpaste to brush kids’ teeth if they’re younger than 3.
    5. For kids who are 3-6 years old, use a pea-size amount of fluoride toothpaste, and supervise these preschool kids when they brush so they don’t swallow too much fluoride toothpaste.

So that’s it! Dental Fluorosis: it’s a scary name, but not a big worry in the U.S.

Whew! One less “-osis” to freak out about!

Subscribe to the Fluoride Exposed newsletter.

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What’s with the anti-fluoridationist promotion of dental health programmes?

“Healthy Teeth, Happy Smile” leaflet promoting dental health programme in Leicester, UK

Anti-fluoride campaigners often promote dental health programmes which they argue are alternatives to community water fluoridation. But seem not to understand that these programmes usually include fluoride dental treatments.

It’s probably a result of some tactical thinking – “let’s promote a positive message to overcome the publicly perceived negativity associated with our opposition to a social health policy like fluoridation.” In fact, some New Zealand anti-fluoride activists have specifically expressed it this way.

But the sting in the tail of this tactic is their promotion of the idea these programmes are an alternative to community water fluoridation (CWF). In reality, they are not genuine about their positive support of a social health policy – they still want to convey a message of opposition to CWF by pretending these policies are successful alternatives.

These programmes may be successful – but they are not alternatives to CWF.  Health authorities promoting them usually see them as complementary to CWF  – certainly not substitutes or alternatives. In fact, these dental health programmes usually include fluoride varnish treatment for children’s teeth.

An example is the “Healthy Teeth, Happy Smile” programme reported as being very successful in the UK city of Leicester. See  City with worst tooth decay in children sees marked improvement). It aims to improve the dental health of young children and includes exercises like supervised tooth brushing in nurseries and linking families up with dentists. The image above shows the first page of a leaflet about the scheme. Notice that it encourages fluoride varnishing of the teeth of young children and offers this free (the image below shows the relevant detail from the leaflet) and yet Fluoride Free New Zealand, the local anti-fluoride group, is promoting it!

The Leicester City Council in its promotion of the scheme lists the following actions for parents:

  • take your child to see the dentist before they are one and go regularly
  • brush your child’s teeth as soon as the first tooth appears
  • brush at least twice a day
  • don’t rinse after brushing just spit the toothpaste out
  • use a fluoride toothpaste
  • ask your dentist about fluoride varnish
  • limit sugary drinks and snacks to meal times only.

The scheme is based on the Oral Health Promotion Strategy for pre-school children which describes its objectives as:

 Optimising exposure to fluoride
 Gain multi-partnership support in order for everyone to play a role in
improving oral health
 Improve preventive and routine dental attendance
 Improve parental skills on caring for children’s oral health

So hardly an alternative to fluoride or CWF.

I have written about other dental health programme which anti-fluoride activists misleadingly promote as alternatives to CWF before.

For example:

The Nexo programme on Sweden – Fluoridation: Open letter to Democrats for Social Credit;

The Scottish ChildSmile programme – ChildSmile dental health – its pros and cons and ChildSmile – a complement, not an alternative, to fluoridation.

I have also made the point that in New Zealand the different District Health Boards often have dental health programmes which incorporate elements of all the three programmes discussed here. They are not run as alternatives to CWF – although some health boards do put extra resources, such a fluoride tooth varnishing into the non-fluoridated areas. For obvious reasons.

Examples are the Mighty Mouth Dental programme run by Counties Manukau District Health Board and the Healthy Smile, Healthy Child programme run by the Ministry of Health and the New Zealand Dental Association.

Whether or not health authorities choose to give their dental health programmes catchy titles such programmes are important. CWF is not a magic bullet and oral health is also served by complementary programmes like these which incorporate education, early training in the use of toothbrushes, connecting families with dentists and use of fluoride varnishes.

Just don’t be fooled into thinking such programmes are substitutes or alternatives to CWF. Especially don’t be fooled by activists who are not seriously promoting dental health but simply attempting to fool people by pretending such programmes could be used instead of CWF.

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Fluoridation not associated with ADHD – a myth put to rest

Fluoridated water is NOT associated with ADHD: Photo by mtl_moe

The myth of community water fluoridation causing attention deficit hyperactivity disorder (ADHD) is just not supported by the data. I show this in a new paper accepted for publication in the British Dental Journal. This should remove any validity for the claims about ADHD by anti-fluoride campaigners.

Mind you, I do not expect them to stop making those claims.

The citation for this new paper is (will be):

Perrott, K. W. (2017). Fluoridation and attention hyperactivity disorder – a critique of Malin and Till. British Dental Journal. In press.

The Background

The fluoridation causes ADHD myth was initially started by the publication of Malin & Till’s paper in 2015:

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.

It was quickly taken up and promoted by anti-fluoride campaigners – becoming one of their most cited papers when claiming harmful psychological effects from fluoridation. Part of the reason for its popularity is that it is the only published paper reporting an association between community water fluoridation (CWF) incidence and the prevalence of a psychological deficit. All other reports on this used by anti-fluoride campaigners are based on studies made in high fluoride regions like China where fluorosis is endemic. Those studies are just not relevant to CWF.

While many critics rejected Malin & Till’s conclusions on the simple basis that correlation does not mean causation I decided to look a bit deeper and test their statistical analyses. This was easy because they used published US data for each US state and such data is available for many factors.

I posted my original findings in the article ADHD linked to elevation not fluoridation. This showed that a number of factors were independently associated with ADHD prevalence (eg., home ownership, poverty, educational attainment, personal income, and % of the population older than 65) and these associations were just as significant statistically as the associaiton reported by Malin & Till.

However, multiple regression of possible modifying factors showed no statistically significant of ADHD prevalence with CWF incidence when mean state elevation was includedd.

The importance of elevation was confirmed by Huber et al. (2015):

Huber, R. S., Kim, T.-S., Kim, N., Kuykendall, M. D., Sherwood, S. N., Renshaw, P. F., & Kondo, D. G. (2015). Association Between Altitude and Regional Variation of ADHD in Youth. Journal of Attention Disorders.

Huber et al., (2015) did not include CWF incidence in their analyses. I have done this with the new paper in the British Dental Journal.

Publication problems

I firmly believe that scientific journals, like  Environmental Health which published the Malin & Till paper, have an ethical obligation to accept critiques of papers they publish (subject to peer review of course). Similarly, it is appropriate that any critique of a published paper is made in the journal where it was originally published. Implicit in this arrangement, of course, is that the authors of the original paper get the chance to respond to any critique and that the response be published by the original journal.

Unfortunately, this was not possible for this paper because the Chief Editor of  Environmental Health,  Prof Philippe Grandjeansimply refused to allow this critique to be considered for publication. No question of any peer reviuew. In his rejection he wrote:

“Although our journal does not currently have a time limit for submission of comments on articles published in EH, we are concerned that your response appears a very long time after the publication of the article that you criticize. During that period, new evidence has been published, and you cite some of it. There are additional studies that would also have to be taken into regard in a comprehensive comment, as would usually be the case after two years. In addition, the way the letter is written makes us believe that the letter is part of a controversy, and our journal is certainly not the appropriate forum for a dispute on fluoride policies.”

My response pointed out the reasons for the time gap (problems related to the journals large publication fee), that no other critique of the Malin & Till paper had yet been published and that any perceived polemics in the draft should normally be attended to by reviewers. This was ignored by Grandjean.

While Grandjean’s rejection astounded me – something I thought editors would consider unethical – it was perhaps understandable. Grandjean is directly involved as an author of several papers that activists use to criticise community water fluoridation. Examples are:

Grandjean is part of the research group that has published data on IQ deficits in areas of endemic fluorosis – studies central to the anti-fluoride activist claims that CWF damages IQ.  He has also often appears in news reports supporting research findings that are apparently critical of CWF so has an anti-fluoridation public standing.

In my posts Poor peer-review – a case study and Poor peer review – and its consequences I showed how the peer review of the original Malin & Till paper was one-sided and inadequate. I also provided a diagram (see below) showing the relationship of Grandjean as Chief Editor of the Journal, and the reviewers as proponents of chemical toxicity mechanisms of IQ deficits.

So, I guess a lesson learned. But the unethical nature of Grandjean’s response did surprise me.

I then submitted to paper to the British Dental Journal. It was peer-reviewed, revised and here we are.

The guts of the paper

This basically repeated the contents of my article ADHD linked to elevation not fluoridation. However, I tried to use Malin &Till’s paper as an example of problems in ecological or correlation studies. In particular the inadequate consideration of possible risk-modifying factors. Malin & Till clearly had a bias against CWF which they confirmed by limiting the choice of covariates that might show them wrong. I agree that a geographic factor like altitude may not have been obvious to them but their discussion showed a bias towards chemical toxicity mechanisms – even though other social factors are often considered to be implicated in ADHD prevalence.

Unfortunately, Malin & Till’s paper is not an isolated example. Another obvious example of confirmation bias is that of Peckham et al., (2015). They reported an association of hypothyroidism with fluoridation but did not include the most obvious example of iodine deficiency as a risk-modifying factor in their statistical analysis

Of course, anti-fluoride campaigners latched on to the papers of Peckham et al., (2015) and Malin & Till (2015) to “prove” fluoridation was harmful. I guess such biased use of the scientific literature simply to be expected from political activists.

However,  I also believe the scientific literature contains many other examples where inadequate statistical analyses in ecological studies have been used to argue for associations which may not be real. Such papers are easily adopted by activists who are arguing for or against specific social policies or social attitudes. For example, online articles about religion will sometimes refer to published correlations of religosity with IQ, educational level or scoio-economic status. Commenters simply select the studies which confirm the bias they are arguing for.

These sort of ecological or corellations studies can be useful for developing hypotheses for future study but it is wrong to use them to support an argument and worse as “proof” of an argument.

Take home message

  1. There is no statistically significant association of CWF with ADHD prevalence. Malin & Till’s study was flawed by lack of consideration of other possible risk-modifying factors;
  2. Be very wary of ecological or correlation studies.Correlation is not evidence for causation and many of these sudues iognore other possible important risk-modifying factors.

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Are fluoride researchers sacked for their findings?

Dr Phyllis Mullenix – employment terminated because of her fluoride research or other reasons? (Image credit: NYC Coalition Against Artificial Fluoridation)

Heard the one about the scientist who was doing excellent research but was sacked by her Institute because her discoveries shattered the prevailing “scientific orthodoxies?”

Yes, it is a common claim. Often made by activists promoting conspiracy theories.  But it is an easy one to make and it is always worth checking the facts in such cases.

Of course, the anti-fluoridation movement is no exception – they claim that a number of “anti-fluoridation scientists” have been sacked for their work. Here I will just look at one of these stories – that of Dr Phyllis Mullenix.

The Mullenix story

A few facts.

Phyllis Mullenix was working for the Forsyth Research Institute in Boston. In her time there, she researched several possible neurotoxicants but made only one study on fluoride which was published in 1995. The paper is:

Mullenix, Phyllis J., DenBesten. Pamela K., Schunior, A., & Kernan, W. J. (1995). Neurotoxicity of sodium fluoride in rats. Neurotoxicology and Teratology, 17(2), 169–177.

This paper has become central to claims made by anti-fluoride campaigners that community water fluoridation lowers IQ in children.

However, this paper is not relevant to community water fluoridation because of the very high concentrations of fluoride used (0, 75, 100, 125 and 175 mg/L in drinking water fed the rats). That such levels are unrealistic was shown by her own report that “the 175 ppm level .  .  . resulted in dehydration and the death of 10 of the exposed animals within 10 days.” Half of the 21 animals exposed died within 10 days!

For comparison, the recommended concentrations for community water fluoridation are usually less than 1 mg/L. But it is interesting that when anti-fluoride campaigners tell Mullenix’s story they rarely mention the concentration she used.

Mullenix did lose her job at Forsyth. A unanimous meeting of senior staff members on April 19, 1994, recommended she not be reappointed to her position. She was a staff associate and employment was usually guaranteed for 12 months at a time. Renewals would have depended on several factors, including the level of funding the employee was able to attract from research grants. Mullenix was informed by letter on May 31, 1994, that the Board of Trustees had approved the recommendation from senior staff members that her appointment would not be renewed.

So, she lost her job – but technically was not sacked – just not reappointed.

Why was her employment not renewed? 

Anti-fluoride campaigners rely on books like “The Fluoride Deception” to support their conspiracy theories

Depends if you believe there was a conspiracy against fluoride research.

Here are some of the conspiracy stories that are floated:

Chris Bryson says in his book The Fluoride Deception:

“PHYLLIS J. MULLENIX. A leading neurotoxicologist hired by the Forsyth Dental Center in Boston to investigate the toxicity of materials used in dentistry. In 1994 after her research indicated that fluoride was neurotoxic, she was fired.”

This claim has been repeatedly presented in articles and submissions by anti-fluoride activists. For example:

She went from being a leading neurotoxicologist at a Harvard affiliated research institute to an industry pariah. This assignment and her findings ruined her career as a grant-funded research scientist.”

Dr Phyllis J Mullenix should be a household name. She was sacked for her work proving Aluminium and Fluoride act synergistically to damage your brain and that of your unborn child.”

Within days of learning that her study was accepted for publication, Dr [Phyllis] Mullenix was fired from the Forsyth Dental Center.  She has received no grants since that time to continue her research.”

Dr Phyllis Mullenix was sacked from the Forsyth Dental Center, where she was head of the toxicology department, for publishing research in Neurotoxicology and Teratology showing that fluoride can adversely affect brain function. She had been warned: “If you publish this information, we won’t get any more grants from NIDR” (from which the institute got most of its money).

And I could go on. And on. There is no shortage of such claims promoted as arguments against community water fluoridation.

But here are some facts.

I have gone to the legal document presented to the US District Court, D, Massachusett on November 13, 1996. These relate to a case brought by Mullenix against Forsyth claiming discrimination and retaliation for her legal actions.

Mullenix’s complaint:

“alleges that Forsyth discriminated against Dr. Mullenix on the basis of her sex, denied her equal pay and one or more promotions and retaliated against her for seeking legal redress during her employment at Forsyth as a Staff Associate from 1982 to 1994.”

The document, Mullenix v. Forsyth Dental Infirmary for Children, is quite long and full of legalese which I would never pretend to understand. But it certainly makes clear that the complaint by Mullenix and the response by Forsyth have nothing to do with fluoride or fluoridation.

Fluoride is mention only a few times:

“Dr. Mullenix asseverates that no one at Forsyth ever questioned the quality of her work or that her fluoride research did not lie within Forsyth’s mission. (Docket Entry # 102, Mullenix Affidavit).”

And:

“Dr. Mullenix contends that Dr. Taubman “called Dr. Mullenix `hysterical’ because he disagreed with her research.” (Docket Entry # 102, p. 18). Dr. Mullenix recites Dr. Taubman’s alleged statement while explaining what she said to Dr. Hay during a conversation a few days after giving a seminar on fluoride research. According to Dr. Mullenix, Dr. Hay mentioned that “Marty Taubman in particular was very irate about the data that was presented …” and that “Marty Taubman had indicated that I was hysterical in my reporting.” (Docket Entry # 98, Mullenix Deposition).”

It appears Mullenix made the complaint about use of the word “hysterical” together with apparently sexist remarks made by colleagues (relating to clothing and the employment rights of women who had husbands) as evidence of a hostile and sexist work environment.

This document outlines the various complaints made by Mullenix – and clearly, they did not relate to fluoride or, directly, to her findings about fluoride. In fact, it says:

“Dr. Mullenix asserts that the only reason other than gender which explains Forsyth’s actions is that it acted in retaliation for Dr. Mullenix’ seeking legal redress.”

Mullenix took her initial legal action because she had been denied a promotion and subsequently claimed Forsyth had retaliated against her because of her initial threat of legal action if her promotion was declined (it was and she did take legal action) and then the actual legal action.

I have focused on Mullenix’s version here because they do make clear that her fluoride research and findings were not involved in any retaliation by Forsyth. The institute’s version, of course, seeks to justify their actions. While there is some reference to her research interest not coinciding strongly with the Institute’s interests, their evidence relates almost completely to salaries for male and female staff members, the responsibilities of the staff associate position that Mullenix occupied, and the extent of funding Mullenix was able to attract.

I have no idea of the legitimacy of Phyllis Mullenix’s complaints or the legitimacy of Forsyth’s rebuttals. Nor do I know what the final outcome of her legal action was.

Mullenix’s complaints could very likely have been genuine. Even today women do get discriminated against in employment and salaries. Their complaints are often disregarded or treated in a sexist way. “Uppity” women can face retaliation. And things are better now than they were in the 1980s and 1990s. It is very likely Mullenix was granted an out-of-court settlement.

But one thing I am sure of – she was not “sacked’ for her fluoride research or publication of her fluoride paper. Any complaint made by colleagues about that work would have been perfectly normal and expected – and she herself, at the time, did not attribute any retaliatory action to her fluoride research.

So, yet another case where it pays to check the claims made by anti-fluoride activists.

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Fluoridation and cancer

Yes, you have. And one lie is the claim that fluoridation causes cancer. Image credit: Have You Been Lied to About Fluoride?

We all know the phrase “Lies, damned lies, and statistics.” If nothing else, this should warn us not to take on faith arguments which rely on statistical analysis for their credibility. Wikipedia uses this phrase to illustrate the “persuasive power of numbers, particularly the use of statistics to bolster weak arguments.”

Unfortunately, the scientific literature is full of weak arguments bolstered by statistics. It’s another case of “reader beware.” Do the statistical analyses used really support the argument? And how good was the statistical analysis anyway?

Unfortunately, scientific papers with poor or inappropriate statistical analyses often get used to bolster arguments in the political field. Anti-fluoride campaigners do this all the time. I illustrated this for the “fluoridation caused ADHD” argument in my articles ADHD linked to elevation, not fluoridation and ADHD link to fluoridation claim undermined again.

Another paper often used by anti-fluoride campaigners is that of Takahasi et al., (2001). They cite this to support their “fluoridation causes cancer” argument. For example, the prominent anti-fluoride activist Karen Favazza Spencer did this recently in a Facebook post quoting from Tkahashi et al., (2001):

“Cancers of the oral cavity and pharynx, colon and rectum… were positively associated with ‘optimally’ fluoridated drinking water.”

Well, how justified is that quote? How reliable was the statistical analysis used by these authors to arrive at that claim?

Takahashi et al., (2001)

In fact, their statistical analysis was poor. They considered only fluoridation as a factor. When we consider other likely factors the statistical analyses show no significant association between these cancers and fluoridation.

Let’s have a look at the paper and the statistical analysis.

The paper is:

Takahashi, K., Akiniwa, K., & Narita, K. (2001). Regression Analysis of Cancer Rates and Water Fluoride in the USA based Incidence on IACR / IARC ( WHO ) Data ( 1978-1992 ). Journal of Epidemiology, 11(4), 170–179.

Briefly, it searched for possible statistically significant associations between the incidence rates for a whole range of cancers and the extent of fluoridation. It used fluoridation extent and cancer incidence data for three US states and six US cities. Other factors were considered only for lip cancer where sunshine extent was included in the analyses.

I set out to repeat their statistical analysis, including some other relevant factors. However, the data they used for cancer incidence in 1978-1992 is not available on-line. But there are data sets available for more recent years.

Here I use the cancer incidence data for 1993-1997 taken from the WHO, International Agency for Research on Cancer publication Cancer Incidence in Five Continents Vol. VIIIThis lists cancer incidence for 58 body sites but I restricted my analysis to eight of the body sites for which Takahashi et al., (2001) reported significant associations with fluoridation.

Are any of these cancers significantly associated with the extent of fluoridation?

Well, yes, two are at the 5% level (p < 0.05) – cancers of the rectum and bladder. The table lists values for the probability p value produced by linear regressions. The p values for cancers at all the body sites considered is also significant – but only for females.

Cancer site p – Male p – Female
Lip 0.750 0.825
Oesophagus 0.427 0.285
Colon 0.090 0.146
Rectum 0.037* 0.048*
Bone 0.784 0.147
Prostate 0.639
Bladder 0.015* 0.031*
Thyroid 0.806 0.519
All sites 0.250 0.020*

Takahashi et al., (2001) found significant associations for rectum and bladder. But also for Colon, bone (male), oesophagus (female), prostate (male) and lip. This difference is not too surprising as I used a different, more recent, data set. Also, correlations do not mean causation, they can occur by chance (1 in 20 samples) and other factors are more than likely involved (see below).

Another difference is that I used simple linear regressions. Takahashi et al., (2001) transformed both fluoridation extent and cancer incidence to logarithms but their explanation for this is inadequate.  Such transformations are not normally applied unless there is evidence that a relationship is nonlinear.  Takahashi et al., (2001) did not give any evidence for this and there was no evidence for it in the data set I used.  Neither was there any evidence of patterns in the residual values from the regression analysis – another sign that simple linear regression was valid.

What about the influence of other factors?

One of the biggest complaints I have about the use of regression analysis in studies like this is that very often other factors are ignored. Takahashi et al., (2001) considered only sun shine extent – and then only for lip cancer.

I think the restriction to consideration of only fluoridation is naive. In fact, probably indicating a bias and a desire to confirm it. It is extremely unlikely that all, or even most, of the specific cancers considered have a single cause – fluoride. And it is unlikely that a single factor would explain all the variability in the cancer incidence data.

Also, fluoride could be acting as a proxy for more relevant factors. The ADHD relationship with the extent of fluoridation is an example. In my paper Attention deficit hyperactivity disorder prevalence associated with altitude but not exposure to fluoridated water*, I showed that fluoridation extent is significantly correlated with mean altitude. When altitude was included in a multiple regression there was no significant association of ADHD with fluoridation.  This suggests that, in fact, the fluoridation data was really a proxy for something else – in this case, altitude – which Huber et al (2015) reported is associated with ADHD prevalence.

I am not intending here to narrow down the most likely factors which are associated with cancer at all these body sites. I simply want to check how significant any association with fluoridation is when other possible factors are included.

Geographic factors are worth considering – not because they necessarily have a direct influence. But because they may act as proxies from environmental, population density and industrial concentration factors which could be important. So I included data for mean elevation, mean latitude and mean longitude together with the extent of fluoridation in multiple regressions of the eight cancers above as well as for all the body sites data.

Using adjusted R square values to test for a fluoridation contribution

Rather than attempting to identify significant correlations with different factors for different cancers, I used the method of judging what effect inclusion of fluoridation extent had on the explanatory power of regression models which included the geographic factors. Jim Frost describes this approach in his article Multiple Regression Analysis: Use Adjusted R-Squared and Predicted R-Squared to Include the Correct Number of Variables

Briefly, he describes problems with the R squared value:

“Every time you add a predictor to a model, the R-squared increases, even if due to chance alone. It never decreases. Consequently, a model with more terms may appear to have a better fit simply because it has more terms.”

Include more factors and you could simply be modelling random noise in the data.But the adjusted R-squared  overcomes this because it adjusts for the number of predictors in a model:

“The adjusted R-squared increases only if the new term improves the model more than would be expected by chance. It decreases when a predictor improves the model by less than expected by chance. The adjusted R-squared can be negative, but it’s usually not.  It is always lower than the R-squared.”

These examples below of multiple regression output including fluoridation and excluding fluoridation in the models illustrate where adjusted R square values are reported:

The table below lists the adjusted R square values for multiple regressions:

  • +Fl included fluoridation extent, mean elevation, mean latitude and mean longitude, and
  • -F included only mean elevation, mean latitude and mean longitude.

Comparing the adjusted R square values for +Fl and -Fl tells us about the effect of including fluoridation extent on the models:

  • Where the value for +Fl is larger than for -F then the extent of fluoridation improves to model more than would be expected by chance.
  •  Where the value of +Fl is smaller than for -F then the extent of fluoridation improves to model less than would be expected by chance.

Male

Female

Cancer site + Fl – Fl + Fl – Fl
Lip 0.170 0.242 0.685 0.649
Oesophagus 0.809 0.842 0.558 0.612
Colon 0.842 0.771 0.681 0.659
Rectum 0.357 0.455 0.616 0.692
Bone 0.451 0.527 0.625 0.700
Prostate -0.350 0.130
Bladder 0.860 0.863 0.530 0.606
Thyroid 0.434 0.544 0.801 0.824
All sites 0.622 0.676 0.846 0.865

The table shows that adjusted R square values are greater (red) when fluoridation extent is not included in the regression model for all cancer sites except the colon and female lip. That indicates that these cancers are not associated with fluoridation extent. That the simple regression results alone  for fluoridation extent in the case of rectum and bladder cancer (and all sites female cancer) are misleading.

The colon and female lip cancer are exceptions – but the fact no significant association was found for fluoridation extent alone (first table) suggests something more complex is occurring here. It could be that the selected geographic factors have very little role in these cancers and inclusion of more relevant factors is needed.

Conclusion

The associations of fluoridation extent with various cancers reported by Takahashi et al., (2001) disappear when we consider other more relevant factors. Therefore, the use of this study by anti-fluoride campaigners to claim fluoridation is responsible for cancer is misleading. Not that I expect, from their past record, they will stop doing this.

More generally this is yet another example showing that readers should beware of putting too much faith in simple statistical analyses reported in scientific papers – even those published in respectable journals. It is just too easy to use statistical analysis to confirm a bias.

We should all keep in mind the phrase  “Lies, damned lies, and statistics” and treat such reports critically. If possibly checking out the extent to which other factors have been considered. Even where significant correlations are reported we should check how useful such correlations are at explaining the variations in the data.


*The full text of this paper is not yet available as it is undergoing journal peer review. However, the full text of CRITIQUE OF A RISK ANALYSIS AIMED AT ESTABLISHING A SAFE DAILY DOSE OF FLUORIDE FOR CHILDREN, the first draft from which this paper was taken, is available.

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