Tag Archives: SciBlogs

The arrogance of science?

IMG_0706

This comment of Richard Feynman’s indicates to me the essential humility of science. Yet we often find that people who seem to subscribe to the support of “answers that can’t be questioned” will accuse science and scientists of arrogance.

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I suspect this is because they have put themselves in the position of being unable to support the claims they are making.

ADHD linked to elevation not fluoridation

Attention-Deficit Hyperactivity Disorder (ADHD) is more likely linked to residential altitude than community water fluoridation (CWF). This finding calls into question a recent paper claiming ADHD is linked to CWF. A paper that is being heavily promoted on social media at the moment by anti-fluoridation groups.

I discussed problems with that paper, (Malin & Till, 2015) in my article More poor-quality research promoted by anti-fluoride activists. Now I have taken my critique further by making my own exploratory investigation of likely influences on the prevalence of ADHD in US states using the approach of Malin & Till,(2015). Except I did not limit my investigation to CWF  data but also included state prevalence data for other likely influences on mental health.

ADHD linked to elevation

Elevation One of the best correlations with ADHD state prevalence I found was with elevation data for each state. It’s a negative correlation – the higher you go the lower the prevalence of ADHD This figure shows the correlation of ADHD state prevalence in 2011 with mean elevation for the 51 states. It is statistically significant with a correlation coefficient (r) of -0.5 and significance (p) of 0.00.

Fluoridation-2010For comparison, the similar correlation of ADHD state prevalence in 2011 with prevalence of CWF in 2010, while significant, has a correlation coefficient of +0.32 and significance of 0.02. However, the correlation with CWF is not significant in a multiple regression with elevation – see below.

Other factors worth considering

My exploratory statistical analysis showed a number of other factors significantly linked to ADHD with correlations similar to, or higher than, CWF. Images for the data and a table of correlation coefficients and their significance are shown below.

The correaltion of ADHD state prevalence in 2011 with home ownership and % living in poverty are better than with CWF. These correlations are positive – the prevalence increases with % home ownership and % of people living in poverty. I guess it is hardly surprising that mental health problems would increase with the amount of poverty. But perhaps in the US home ownership is also not conducive to mental health?

Home-Poverty

The correlations of ADHD state prevalence with educational attainment (Bachelors degree) 2009 and Per Capita personal income 2010 were similar to that with CWF. These correlations are negative – I guess its easy to understand that higher incomes and better education is conducive to better mental health (lower prevalence of ADHD).

Education-Income

over-65

The correlation of ADHD state prevalence with the proportion of the sate’s population older than 65 was also similar to that for CWF. The correlation is positive and one can only speculate on reasons for the increase of ADHD prevalence as the proportion of older people increases.

The table below summarises correlation coefficients (r) and statistical significance (p) for the figures above.

Correlation of ADHD state prevalence with a range of factors

State data Correlation coefficient (r) Statistical significance (p)
Mean elevation -0.50 0.009
CWF 2010 % +0.32 0.022
Home ownersip % +0.38 0.005
Poverty % +0.37 0.007
Education (% Bachelor’s degree) -0.35 0.011
Per capita income ($) -0.32 0.022
Age over 65 % +0.30 0.031

Multiple regressions

CWF in 2010 is correlated with mean elevation – correlation coefficient r=-0.43 and significance p=0.002 – suggesting these are not independent variables. (CWF in 1992 was similarly highly correlated with mean elevation.) Perhaps Malin and Till (2015) only found a correlation of ADHD with CWF because they are both related to mean elevation.

Multiple regression analysis suggests this is the case. The statisitically significant factors were mean elevation (p=0.001), home ownership (p=0.000) and poverty (p=0.005). The contribution of CWF in 2010 was not statistically significant in this multiple regression (p=0.587) as were most of the other factors I considered.

Malin and Till (2015) use the CWF for 1992 in most of their comparisons. My analysis shows this has a better correlation with ADHD prevalence in 2011 than CWF for any other year (r=0.45 cf 0.32 for CWF in 2010). It seems strange to use 20 year old data in  a model predicting ADHD prevalence for 2011 so I used more recent data for my exploratory analysis. However, in a multiple regression the contribution from CWF in 1992 was still not statistically significant (p= 0.158).

Conclusion

We should be careful of conclusions arising from such exploratory investigations. Firstly the obvious – correlation is not causation. But secondly the choice of data  is crucial.

Malin and Till (2015) chose to consider CWF prevalence as the main factor influencing ADHD prevalence. They did also include socioeconomic status (SES) as a secondary factor.  However, my analysis shows a number of other factors which could equally be considered. And when they are considered in multiple regressions the contribution from CWF is not statistically significant.

modelThe model used by Malin and Till (2015) using CWF in 1992 and SES in 1992 explained only 31% of the variance of ADHD prevalence in 2011. The corresponding firgures for ADHD prevalence in 2003 and 2007 were 24% and 22%.) But using a model for the influence of mean elevation, home ownership and poverty only (no CWF included) I was able to predict the state prevalence of ADHD in 2011 as shown in this figure. This accounts for 48% of the variance and has a significance of p= 0.000. Perhaps further exploration of the available data could produce an even better model but the key point here is that CWF does not contribute anything once mean elevation is included.

I do not think Malin and Till (2015) are justified in drawing the conclusion that CWF influences ADHD. Their mistaken conclusion has arisen from their limited choice of data considered for the exploratory analysis. That in itself seems to have resulted from a bias inherent in their hypothesis that “fluoride is a widespread neurotoxin.”

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More poor-quality research promoted by anti-fluoride activists

Anti-fluoridation propagandists must think all their Christmases have come at once. They at last have a “peer-reviewed” scientific paper they can claim supports their position. What’s more, it is the second such paper to appear in the last month.

But they really are resorting to arguments of quantity (2 papers) over quality. This new paper claiming a link between community water fluoridation (CWF) and Attention-Deficit Hyperactivity Disorder (ADHD) is of just as poor quality as the earlier one claiming a link with hypothyroidism. Both papers are speculative, ignore other relevant factors, and “prove” nothing.

I discussed the hypothyroidism paper in the article Paper claiming water fluoridation linked to hypothyroidism slammed by experts. The new ADHD paper is:

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.

Here are my thoughts on this paper.

Exploratory investigation – correlation not causation

The authors have simply taken existing online data and searched for a statistically signficant relationship. They have explored the limited data sets used – not attempted to prove an effect. After all, correlation does not prove causation – the graph below shows an example of how correlation can often produce meaningless results.

The data sets Malin and Till (2015) used are both from the USA Centers fo disease Control (CDC).

  1. State-based attention-deficit hyperactivity disorder (ADHD) prevalence (Visser et al., 2014);
  2. Numbers of people receiving fluoridated water from public water supplies in each state obtained from the CDC.

Note, they did not use data for individual children exhibiting symptoms of ADHD  determined by  a health professional. The data was from random surveys “in which parents were contacted via telephone and asked about the emotional and physical well-being of a randomly selected child from their household.” Similarly they did not use data for dietary intake of fluoride by individual children but used “the percentage of the U.S. population on public water systems that receives optimally fluoridated drinking water.”

They have assumed these data are reliable proxies for occurrence of ADHD and fluoride dietary intake. But the data could represent other factors as well.

For example, parental reporting of ADHD could differ from state to state because of differences in parental educational levels and ideological attitudes. People in  different sates may not have the same level of knowledge, awareness or acceptance of such behaviours. Malin and Till themselves acknowledge ADHD reporting is higher for parents with a high school education than for parents who did not graduate high school (Visser (2014). Parental education levels are likely to vary from state to state.

The availability of CWF can be dependent on the size of urban areas for both technical reasons and because of  recognised willingness for innovation from large and high status city leaders (Crain, 1996) so that the state prevalence used could be acting as a proxy for the distribution of urban areas of different sizes, and the relative urban/rural distributions in different sates. A correlation may indicate nothing more than a relationship between city sizes and parental education.

The authors themselves warn their study has limitations, saying it is:

“an ecological design that broadly categorized fluoride exposure as exposed versus non-exposed rather than collecting information related to concentration of fluoride and patterns and frequency of exposure or outcome at the individual level. Future research could explore the relationship between exposure to fluoridated water and the occurrence of ADHD at the individual level.”

And, again, we should always keep in mind that correlation does not prove causation.

The starting hypothesis

Inevitably any serious exploratory investigation should start with a working hypothesis. As psychologists the authors are presumably interested in ADHD and its causes. But why investigate state prevalence of CWF instead of any of the other factors indicated in this condition. In fact they list a range of candidates from arsenic and lead to food additives and food colouring. Granted, they saw CWF as a field ripe for plucking as they say fluoride “has received virtually no attention in the ADHD literature.” But I would have expected them to at least include these other known factors as confounders in their study.

I think the answer lies with their biased reading of the literature. They start with the claim that fluoride is a “widespread environmental neurotoxin,”  but only really cite Grandjean and Landrigan (2014) and the closely-related meta-analysis of Choi et al., (2012) to support this claim. I have discussed those papers and their problems in  Repeating bad science on fluoride and Controversial IQ study hammered in The Lancet. A major problem with that work is it involved areas of endemic fluorosis where fluoride intake is high so it is not directly relevant to CW. In fact, the authors’ bias is indicated by the fact they did not cite Broadbent et al., (2014) which showed no neurotoxic effects of CWF. Broadbent et al.’s paper is directly relevant to CWF – Choi et al.’s is not. (I discussed the differences as indicated by dental fluorosis data in my article Water fluoridation and dental fluorosis – debunking some myths

I feel this omission indicates that the authors resort to the special pleading of anti-fluoride activists in the citations they used for justifying their starting hypothesis. The also rely on studies of rats fed very high levels of fluoride, such as that of  Mullenix et al., (1995), and then use her weak argument to claim relevance to CWF by comparing  rat blood plasma F levels to those for humans ingesting high levels of fluoride. (See my article Peer review of an anti-fluoride “peer review” for a discussion on this). Similarly, although acknowledging the high F intake levels of most of the studies reviewed by Choi et al., (2012), they excuse this by referring to the one study with low levels (0.88 mg/L) – ignoring the fact this was a one and a half page article in a newsletter describing measurements in an iodine deficient area. In this study (Lin, et al., 1991) children from low iodine areas were compared with a group from another area that had received iodine supplementation. About 15% of the children suffered mental retardation, 69% of these exhibited subclinical endemic cretinism. The effect of iodine supplementation was clear, the effect of fluoride not so clear. (See Peer review of an anti-fluoride “peer review” for further discussion of this).

So, I think the justification for their starting hypothesis is hardly objective

“Natural” vs “artificial” fluoride

Despite  problems with justification for their hypothesis they did find a significant positive relationship between the US state prevalence of parent-reported ADHD in children and the state proportion of water supplies with optimum levels of fluoride. Again, not a proof of their hypothesis, but interesting data to consider nonetheless. They found inclusion of socio-economic status data improved the relationship but did not consider other relevant confounding factors like parental education and exposure to relevant chemicals.

In contrast, the relationship they found between ADHD prevalence and natural fluoride prevalence (at optimum level or above) was negative and statistically signficant. This actually conflicts with their starting hypothesis of chemical neurotoxicity based on the work of Choi et al., (2014) and Grandjean and Landrigen (2014). While they concede the data really doesn’t allow a conclusion they suggest it could result from the ADHD effect being specific to “fluoridation chemicals” and not fluoride itself.

This leads them to suggest a theoretical “pathway” for CWF contributing to ADHD – the corrosion of lead-bearing plumbing by fluorosilicic acid. Trouble is this ignores the well established fact that fluorosilicates used in CWF decompose to form silica and the hydrated fluoride anion when diluted in water. Malin and Till seem oblivious to work showing this and rely instead on citation of the poor quality work of Masters and Coplan to support this “pathway.” Another example of their citation bias.

But their proposal does raise an important question. Given that lead is one suggested cause of ADHD why did they not concentrate their exploratory analysis of data for lead intake by children in different states, rather than CWF prevalence? Or at least include lead levels as confounders in their statistical analysis.

The thyroid story again

Their second suggested “pathway” is via suppression of thyroid gland activity by fluoride. But, again, this hypothesis does raise the question of other causes, in particular iodine deficiency. (See my discussion of Peckham’s paper – Paper claiming water fluoridation linked to hypothyroidism slammed by experts – for more on this). If this was part of their starting hypothesis then why not consider data for state prevalence of iodine deficient diets of children? Or or include this as a confounder in the analysis?

I find it interesting that despite declaring a starting hypothesis based on the chemical toxicity claims of Choi et al., (2012) and Grandjean and Landrigen (2014), Malin and Till have not proposed any theoretical “pathway” involving direct neurotoxicity of fluoride itself to explain their result. This makes their unwillingness to consider other relevant confounding factors even more obvious.

Conclusions

As I wrote above correlation is not causation  and this study does not “prove” anything. The observed “link”could represent a number of other relationships which are not directly associated with CWF. The analysis also suffers from a lack of consideration of obvious confounding factors.

I believe this is the sort of problem that arises when researchers have a committment to a starting hypothesis and peer review systems are inadequate. Such studies are a problems when published because ideologically motivated activists love to cherry-pick them to claim “scientific support” for their cause. This is not helped when the researchers themselves climb on the activist bandwagon and attempt to claim more for their findings that is really justified.

I think Malin and Till have done this with the press release from their department – Fluoride in tap water associated with ADHD in children, researchers find. It is one thing to say:

“Our findings showed that artificial fluoridation prevalence in 1992 predicted ADHD prevalence in 2003, 2007 and 2011 among children and adolescents in the United States, and that was after controlling for median household income.”

But the careful claim their “findings showed” a “prediction” is far too easily seen as proof in the mind of the lay-reader. Worse, they draw unwarranted conclusions from their limited work:

“As citizens of Toronto, living in an artificially fluoridated community, I think we need to ask ourselves whether this is still a worthwhile practice.”

One can only pose such questions in the context of an objective assessment of their own work together with other research of possible harmful and beneficial effects of CWF. I think their biased choice of citations in this paper shows they are not capable of doing this.

On the other hand reviews such as the recent NZ Fluoridation Review, Health effects of water fluoridation : A review of the scientific evidence, have done this. Community leaders should be going to such sources for their information and not rely on cherry-picked poor quality studies like Malin and Till (2015) which will be promoted to them by anti-fluoride propagandists and activists.

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Free download – “Severe dental fluorosis and cognitive deficits”

S08920362Anyone interested in my article on this subject in Neurotoxicology and Teratology can now download a pdf version:

Perrott, K. W. (2015). Severe dental fluorosis and cognitive deficits. Neurotoxicology and Teratology, 48, 78–79.

The publishers tell me that anyone who clicks on the link until May 3, 2015, will be taken to the final version of on ScienceDirect for free. No sign up or registration is needed – just click and read!

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Are submissions on fluoridation worth it?

Like most people I struggle to find the energy when representative and government bodies call for submissions. But I did make the effort recently when Medsafe called for submissions on their proposed clarification of how fluoridating agents are defined in the medicine regulations. I am pleased to see the simple suggestion I made was accepted. But my purpose here is to illustrate how this consultation proceeded and how opponents of community water fluoridation (CWF) tried to swamp it with their submissions.

The background

Last November the Ministry of Health (MoH), through Medsafe, called for submission on a change to the Medicine Regulations 1984. This change had been recommended by the High Court and the Crown Law Office who specifically suggested that fluoride compounds used for CWF be exempt from definition as a “medicine.” This arose from the defeat of attempts by an anti-fluoride group, New Health NZ, to use the argument that fluoridation was medication in the High Court actions against CWF. Despite these defeats the High Court and Crown Law Office considered the regulations should be clarified to remove the argument from repeated litigation.

Simply, the proposal was to add a new regulation:

“Fluoride-containing substances, including the substances hydrofluorosilicic acid (HFA) and sodium silico fluoride (SSF) are not medicines for the purposes of the Act when they are manufactured and supplied or distributed for the purpose of fluoridating community water supplies.”

Medsafe asked for responses to the following questions:

  • Question 1: Do you support the proposed amendment? If not why not?
  • Question 2: Are there other fluoride-containing compounds used to treat community water supplies that should be specifically named in the regulation? If so, what are they?

Submissions – quantity or quality

The report from MoH on the process and their recommendations to cabinet give an idea of the submissions made and the final decision.

As we might expect from past experience the submissions were dominated, in numbers if not quality and relevance, by those from the anti-fluoride groups. They had organised a national and international campaign to swamp Medsafe. Paul Connett’s Fluoride Action Network, Fluoride Free NZ and New Health NZ even provided texts and templates to copy and paste into submissions.

Here is the description of the consultation outcome in the MoH report:

MOH-report-extract

So, the activist organisations can certainly mobilise their forces for submissions. But concentration on numbers and not content – and cynical provision of content to followers anyway – didn’t win them any credence. Did they really think blatant duplication of submissions would not stick out like a sore thumb?

It is also heartening to see that the MoH was not swayed by blanket repetition of arguments which do not have credible scientific support. (I guess we can also see why the anti-fluoride activists groups are putting so much effort into their campaign to attack and discredit the NZ Fluoridation Review which summarises the scientific evidence.)

Sometimes suggestions are accepted

I had made the simple suggestion tha sodium fluoride be added to the short list of examples of fluoride chemicals used for CWF. So this recommendation to cabinet pleased me

recommend-to-cabinet

Nice to know that the consultation was not a sham and that reasonable and credible suggestions were listened to and even accepted. It is worth making submissions even when one is aware they me in a minority. If something is worth saying it should be said despite attempts by others to confuse issues.

Also nice to know that some consultations are not simply swayed by quantity and not quality – as was the case for the Hamilton City Council fluoride consultation in 2013 (see When politicians and bureaucrats decide the science).

The Hamilton City Council consultation also showed an extreme naivety in the Council’s willingness to ignore the established science. I wonder what approach they would have taken if the NZ Fluoridation Review had been available at the time?

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Social media and science – the problems and the challenge

Social media – Facebook, Twitter, etc., – are a challenge for science.  Often considered frivolous or at least not serious, they are tempting to ignore. But it seems that many anti-scientific or pseudoscientific ideas a promoted by social media. What’s more, these new social media are very effective at promoting messages, especially in areas of social health, so we ignore the media at our peril. Social media are a fact of modern life and if we can’t beat them, perhaps we should use them ourselves. These are the messages I got from a recent study of the way public health misinformation is promoted via social media. The paper is:

Seymour, B., Getman, R., Saraf, A., Zhang, L. H., & Kalenderian, E. (2015). When Advocacy Obscures Accuracy Online: Digital Pandemics of Public Health Misinformation Through an Antifluoride Case Study. American Journal of Public Health, 105(3), 517–523.

Although limited to an anti-fluoride Facebook case study I believe that the findings are also applicable to other anti-scientific movements like anti-vaccination and climate change denial. Here are some of the findings in the paper.

Anti-fluoride Facebook groups are highly connected

The connectedness within and between anti-fluoride networks was measured to get an idea of their social influence. networks Facebook “friend” connections between members within groups and between groups was very common and overall the study sample showed a significantly higher degree of connection than in Facebook overall. This is probably the result of group members having similar ideology or other traits leading to a desire to form social connections. Social influences lead to group shaping of individual attitudes and behaviours related to health and not reliance on expert findings.

Social diffusion of scientific misinformation

Using an original source article the authors followed posts about the article to determine the degree of social diffusion. They found 60% of the time a reader would have to follow 2 to 3 links to arrive at the original source with such a search failing 12% of the time. This demonstrated that:

“on average, there was a high risk that antifluoride Facebook group members engaged in posts about the article would be forced to navigate through multiple pages to locate the original post or would never succeed in locating it at all, greatly increasing the likelihood for the spread of misinformation and misrepresentation of the scientific article’s content.”

Although not detailed in the paper I believe that key sources of primary information for such social networks is very often articles in the “natural” health or alternative health magazines and websites which have already misinterpreted and misreported the scientific literature.

Engagement and sentiment

The levels of engagement and sentiment of the most influential posts were analysed:

“to explore the user experience with social diffusion of information and to determine how these posts could potentially influence group member attitudes and behaviors. Considering the distance between reference posts and the original source, this is particularly important.”

The figure below illustrates their finding for  the 2 most influential posts in the social diffusion map. Interestingly:

“The most frequent type of comment about the posts and the type of comment that received the most engagement were the science-based comments . . . Science-based comments overall received a positive (profluoride) total sentiment score of 36 (additive over all comments), whereas all other types of comments received an overall negative (antifluoride) sentiment score of –47.”

Seymour-3

“These results demonstrate that the user experience, when engaging with these influential posts, is just as likely to be negative and irrelevant to the original source as it is to be positive and reference scientific information (accurate or not). Our results demonstrate a high probability (1 in 2 chance) of encountering negative and non-science-based information about fluoride that is unrelated to the original peer-reviewed scientific publication under discussion.”

Social media overriding traditional health communication?

The new social media have given a new power to social networks:

“Historically, naturally limiting factors such as geography and communication barriers inhibited opportunities for strengthening networks with outlying views. Risky behaviors as a result of shared moral evaluations, such as opting out of  recommended childhood vaccination schedules and rejecting fluoridation, reverberated in existing small networks without necessarily scaling to dangerous magnitudes.”

But:

“online social networking allows greater connectivity among networks through the increased visibility of group behavior; previously nonnormative behaviors can thus become normative through the use of social media.”

Now that minority ideas and behaviours have an online market they can spread through confirmation bias and the expanding social networks, and the strong ties in the networks reinforce the sentiments behind the spreading messages.
The group thinking and the “silo,” even protective,  nature of social networks means that:

“Expert opinion grounded in evidence that contradicts the sentiments embedded in a socially diffused message will be quickly rejected; acceptance of this contradictory information would be socially detrimental to the network, challenging its very identity. Thus marks the beginning of digital pandemics of misguided and incomplete health information in which evidence becomes entirely secondary to the sociology of the networks diffusing it.”

Are there lessons here for pro-science groups?

The findings of this research will strike a chord with sceptics and others who fight anti-evidence-based approaches to health online. They will easily recognise the social norms of such groups which leads to rejection of any attempt to inject a pro-science discussion. They will have experienced the put-downs and banning or blocking used to reinforce and protect those within-group social norms.
But should we be drawing lessons from this? The authors conclude:

“Traditional vertical health communication strategies, such as broadcast diffusion through peer review publication and media reporting, may no longer be effective because of the existence and viral potential of social diffusion”

Perhaps we have to accept that:

“the sociology of networks is perhaps just as influential as, if not more influential than, the information content and scientific validity of a particular health topic discussed within and between certain networks via social media.”

Rather than trying to beat this new technology perhaps we should try to use it ourselves more effectively. The authors suggest:

“Empirical social strategies for health communication should focus not only on high-quality digital information production and dissemination but also on socially targeted and custom-designed messaging that conforms to the norms and values of specific target networks rather than challenging them. Developing an appreciation for the sociology of target groups could assist public health experts in increasing influence in problem networks and could provide the tools to predict, prevent, or reverse digital pandemics.”

The internet has forced changes on the traditional methods of information dissemination in other areas so it is really not surprising to expect it to change scientific and public health communication. As the authors say in their final words:

“The public nature of social media is at once a barrier to accurate information flow online and a tremendous opportunity for public health research, innovation, and intervention. In an age when negative digital pandemics can go viral, public health communication management strategies must go social.”

See also: An emerging threat of “digital pandemics”- lessons learned from the anti-vaccine movement
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February ’15 – NZ blogs sitemeter ranking

blog-breakdown

Image credit: Dear Kitty. Some blog

There are now over 300 blogs on the list, although I am weeding out those which are no longer active or have removed public access to sitemeters. (Let me know if I weed out yours by mistake, or get your stats wrong).

Every month I get queries from people wanting their own blog included. I encourage and am happy to respond to queries but have prepared a list of frequently asked questions (FAQs) people can check out. Have a look at NZ Blog Rankings FAQ. This is particularly helpful to those wondering how to set up sitemeters.

Please note, the system is automatic and relies on blogs having sitemeters which allow public access to the stats.

Here are the rankings of New Zealand blogs with publicly available statistics for February 2015. Ranking is by visit numbers. I have listed the blogs in the table below, together with monthly visits and page view numbers.

Meanwhile I am still keen to hear of any other blogs with publicly available sitemeter or visitor stats that I have missed. Contact me if you know of any or wish help adding publicly available stats to your bog.

You can see data for previous months at Blog Ranks

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Paper claiming water fluoridation linked to hypothyroidism slammed by experts

“As epidemiological evidence goes, this is about as weak as it gets.”

Author Stephen Peckham – former chairperson of activist group “Hampshire against fluoridation”

That is the comment by Prof David Coggon, Professor of Occupational and Environmental Medicine, University of Southampton, on a new paper claiming hyporthyroidism is linked to water fluoridation. Published yesterday in the peer-reviewed Journal of Epidemiology & Community Health, the paper is:

Peckham, S., Lowery, D., & Spencer, S. (2015). Are fluoride levels in drinking water associated with hypothyroidism prevalence in England? A large observational study of GP practice data and fluoride levels in drinking water. J Epidemiol Community Health, 1–6.

Prof Coggan goes on to say:

“Essentially the researchers have shown that after limited adjustment for demographic differences, there are somewhat higher rates of hypothyroidism (which can result from a number of different diseases) in four areas of England that have higher concentrations of fluoride in drinking water.   It is quite possible that the observed association is a consequence of other ways in which the areas with higher fluoride differ from the rest of the country.  There are substantially more rigorous epidemiological methods by which the research team could have tested their idea”

Having read the paper I think that about sums it up.

Critical role of iodine.

The authors acknowledge that iodine plays a key role in thyroid status but they did nothing to include dietary intake or deficiency in their statistical model. It is just not good enough to declare “it is unlikely that there are significant differences [in dietary iodine intake] between people, living in fluoridated and non-fluoridated areas.”

They did include data for the proportion of people over 40 and the proportion of females because they recognised age and gender influence the incidence of hyperthyroidism. So why not include dietary iodine which is recognised as the main factor? And they are arguing that fluoride potentially acts as an iodine inhibitor, making the data for iodine even more important. Perhaps this data was not so easy to find – but did they look very hard?

Correlation is not causation

This cannot be repeated often enough. Trouble is that almost anyone can get hold of data these days and force it through a statistical package. And if they have a bias to confirm, and are willing to select their data and avoid confounders, they might get lucky.

This seems to be the case here as the senior author is a well-known anti-fluoride campaigner in the UK.* This is outside his specialty (health policy, not epidemiology).

Fluoridation data is readily available for cities and regions but it can easily be a proxy for more meaningful information like the size of towns (smaller towns usually don’t have artificially fluoridated water) or rural/urban distinctions. Cultural and ethnic factors may also be reflected in fluoridation data.

In this case, Peckham et al., (2015) simply correlated the incidence of hypothyroidism reported by individual medical practices against drinking water fluoride concentrations reported by local bodies in the region. There was no attempt to match data at the individual level. And there was no attempt to include dietary iodine intake as a factor – despite its key importance.

The size of the effect

The prevalence of hypothyroidism in the data they used is relatively low  – 3.2% with a standard deviation of 1.1%. The authors argue their results would mean that fluoridation would increase this small number by a small amount (about 30%).

Given the tentative nature and unreliability of their conclusions – if only because they did not consider dietary iodine as a factor – their recommendation should be taken with a grain of salt (preferably iodised). They recommend:

“To minimise the risk of increasing the prevalence of hypothyroidism, it is important, therefore, to limit fluoride ingestion from all sources.”

Sensible health authorities will balance the low incidence of hypothyroidism and the small effect Peckham et al (2015) claim, based on their unsatisfactory analyses, against the fact of the beneficial role that fluoride plays in the oral health of most people throughout their lives

Obviously authorities are no going to change their views as a result of this paper. Of course there will be special pleading by those opposed to fluoridation. They will argue that despite the problems with this paper the questions of fluoride as a factor in hyperthyroidism should be research further. Of course it should – scientific conclusions are always open to being altered by new evidence. But future research must be of a better quality than this. As a Prof Coggan says:

“There are substantially more rigorous epidemiological methods by which the research team could have tested their idea”

Stephen Peckham is a well-known anti-fluoride activist

I discussed Stephen Peckham in a earlier article Peer review, shonky journals and misrepresenting fluoride science. This deals with a previous paper of his and the journal he published it in.

That paper was a collection of the usual anti-fluoride arguments – based in citations without any original work. It was published in a shonky journal known to have poor peer review standards.

The current paper is in a reputable journal and does include some original work – although it is basically a statistical analysis of readily available data. No effort seems to have been made to include data for dietary iodine intake which I would think is a basic need for such a study. I am personally surprised the reviewers used by this journal did not seriously question the paper’s publication for that reason alone. I guess this reflects the imperfect and human nature of peer review even in good science journals.

At least with the current paper Stephen Peckham has declared  a conflict of interest involving his activity opposing water fluoridation – this did not happen with his earlier paper.

I expect this new paper will become another weapon in the anti-fluoridation artist armoury. It will be cited and presented as absolute proof that fluoridation is bad for our thyroids. Claims will be made that a leading scientific journal and university officially claim this! Harvard University and The Lancet all over again.

But sensible readers should never take such claims at face value. Just because a paper is published in a reputable peer-reviewed journal does not make it gospel truth. Whatever the source, such papers need to be considered intelligently and critically.

This paper does not live up to the claims the anti-fluoride propagandists will make about it.

See also:

Flawed study overstates link between fluoride and ill health: experts
Tournage de la scène «Fluoration de l’eau», prise 2793… (Shooting the scene “Water fluoridation,” taken in 2793)

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NZ Fluoridation review – Response to Micklen

I welcome open and transparent discussion here so am thankful to Dr Micklen for his response (see NZ Fluoridation review – HS Micklen responds to critique). Unfortunately he is the only author or “peer-reviewer” of Fluoride Free NZ’s report criticising the NZ Fluoridation review to accept my offer of a right of reply to my critiques.

A pity, as if any of them think I have got things wrong, and they can support this with evidence, I certainly want to know about it.

There are three aspects to Dr Micklen’s reply – dental fluorsis chronic kidney disease and his critique of my letter in the journal Neurotoxicology and Teratology –   Perrott (2015). I will deal with these separately.

Dental fluorosis

I appreciate Dr Micklen is unhappy about my criticisms of his article, and my suggestion his comments of dental fluorosis were muddled. I may have been a bit harsh but he has still not responded to my specific criticism that he:

“unfairly attributes the more severe forms [of dental fluorosis] to community water fluoridation (CWF). Consequently he calculates a cost of dental treatment which is wrong.”

The key problem is that Micklen is assuming that all the  medium and severe dental fluorosis can be attributed to CWF, whereas none of it can.

Briefly reviewing the argument – the figure below is from the NZ Ministry of Health’s Our Oral Health – the same source Micklen used.

My comment on the relevance of the different grades of dental fluorosis was:

“Moderate and severe grades of dental fluorosis are common in areas where fluorosis is endemic, but relatively rare where CWF is used. Occurrences in the latter case, despite the low concentrations of fluoride in treated drinking water, will have other causes – high natural levels in well water, industrial pollution, excessive consumption of toothpaste, etc.”

The important factor is that severe and moderate forms of dental fluorosis are not caused by CWF.

CWF can contribute to mild and very mild forms of dental fluorosis but because these are usually judged positively they certainly don’t need expensive veneers – my dentist colleagues advise simple microabrasion usually works.

So Micklen was wrong to suggest the cost of cost of veneers (up to $1750 per tooth) should be attributed to CWF because such costs would be encountered in non-fluoridated areas as well.

(In fact, if Micklen had calculated costs for such treatment in non-fluoridated areas using the “Oral Health” data in the literal way he did for the fluoridated areas,  he would have found costs to be higher than in non-fluoridated areas! Certainly doesnt’ support his claim but a meaningless result because of the small numbers and large variability).

Chronic kidney disease

Micklen accuses me of  using “a piece of grammatical legerdemain to pretend that I [Micklen] called for CKD sufferers to be warned to avoid tap water, which I did not.”

Granted he left himself a way out by actually writing:

“I suspect that most opponents of fluoridation would call for CKD sufferers to be warned to avoid tap water. Possibly the NZ health authorities have done so.”

OK, so its not a direct personal recommendation (perhaps he doesn’t belong to the group of “most opponents of fluoridation”) but a reader could be excused for getting that message and in this context it comes across as “dog whistling.”

However I will accept his assurance now that:

” In fact, I am inclined to agree with him [me] that that might be extreme in the present state of knowledge.”

As for questions like: “Does further research on the topic receive any funding priority, for example?” – well this is a round about way of giving the message that it doesn’t. Perhaps he should actually check that out and give some evidence instead of making an unwarranted implication.

This tactic of posing unfounded questions to convey an unwarranted message is typical of the approach Micklen and Connett take in their book The Case against Fluoride. I criticised this tactic in my exchange with Paul Connett (see Fluoride Debate).

I reject Micklen’s suggestion that:

“Perhaps it would be embarrassing, too, for a government to insist on putting fluoride in the water and then advise a substantial number of people not to drink it – or so one might think.”

That is silly – it is like a conspiracy theory. Why would genuine health authorities refuse to give warnings to a small group of people who might be put at risk from a social health policy that is beneficial to the vast majority? Surely they are used to such situations.

I also think he is waxing lyrical with the word “substantial!” The numbers involved would be very small, if any, and such a group would already be advised about a number of risks to them because of their condition and treatments.

Micklen also lets his ideological position take over  by drawing the implication from my article that I am saying CWF is “effective and safe – for some.” Far from it. Surely I am saying it is effective and safe for the vast majority (which is what we can expect from a social health policy) and simply recommending (as in all such policies) that the small group of people, if any, who might be at risk should use alternatives.

I am actually saying that CWF is effective and safe for at least  the vast majority and that claims to the contrary should be backed up with evidence which should be considered critically

Severe dental fluorosis and cognitive deficits

I thank Dr Micklen for his comments on my letter in the journal Neurotoxicology and Teratology – (Perrott 2015). I am pleased he accepts the hypothesis that severe dental fluorosis could explain observations of cognitive deficits is worth considering and  he agreed with the other reviewers the letter was worth publishing.

Influence of age

I take his point that the poor appearance of teeth may not influence young children (ages 6-8 as in the small the group Choi et al, (2015) studied). However, this is pure speculation on his part and is surely a detail. A detail that should be considered in any planned research incorporating this hypothesis, but not in itself a reason for rejecting the hypothesis out of hand – surely?

Unless, of course, he can give evidence to support his suggestion. I notice that he does not support the idea with any citations so suspect the idea is more one of straw-clutching  than a serious suggestion.

Actually most, but not all, of the citation I used did indeed refer to work with older children. Some were review papers and did not limit their review to any age group. Aguilar-Díaz, et al., (2011) considered children from 8 – 10 years old, Do and Spencer, (2007) studied 8-12 year olds and Abanto et al., (2012) 6-14 year old children. Chikte (2001) studied three groups: 6, 12, 15 year olds.

However, I found a quick literature search showed reports of negative effects of oral defects like tooth decay on the child’s quality of life. Kramer et al., (2013) reported this for ages 2 – 5, Scarpelli et al., (2013) for 5 year olds and Cunnion et al., (2010) for 2 – 8 year olds.

So, I suggest on the available evidence the negative influence of severe dental fluorosis on quality of life (and possibly cognitive deficits) is likely to occur even in younger children who have not “reached an age to be self-conscious about their appearance.”

I don’t think young children are as immune to social attitudes and personal appearance as Dr Micklen suggests.

Does effect depend on how common dental fluorosis is? 

Dr Micklen suggests that:

“Since fluorosis was common in the community [the children studied by Choi el., 2015], having the condition would not appear abnormal.”

Again I think he is indulging in straw-clutching, or special pleading.

special-pleading-fallacy

Clearly medium and severe dental fluorosis is far more common in this Chinese group than in countries like New Zealand which use CWF. In the graph below I compare their data with that for New Zealand and USA. Incidentally, this figure shows why the data from Choi et al., (2012, 2015) should not be used as an argument against CWF – yet that is what Micklen did in his original article.

DF---good-and-bad

But this does not mean that those children with more severe forms will not stand out against the children with less severe forms. There is always a range of appearances of such defects in a group of children. Some will obviously suffer more than others because of their appearance.

If Choi et al., do continue to include detailed analysis of dental fluorosis in their future work on this issue then it will be possible to compare cognitive deficit measurements with dental fluorosis indices in a larger group. Such data will be interesting.

However, discussion of details like this is premature. My letter simply raised to idea as an alternative worth considering and encouraged the group to continue including detailed dental fluorosis measurements in future work. I was also concerned that they were not being sufficiently open-minded in their choice of a working hypothesis. I concluded my letter with:

Researchers need to be careful not to limit their possible hypotheses or research approaches. Unfortunately Choi et al. (2014) appear to be doing just this with their plans for a larger scale study targeted only at “fluoride’s developmental neurotoxicity.”

Unfortunately none of this group have yet responded to my letter.

So, again, I thank Dr Micklen for his feedback on that letter – and his acceptance of the right-of-reply to my article critiquing the FFNZ report.

See also:

References

Abanto, J., Carvalho, T. S., Bönecker, M., Ortega, A. O., Ciamponi, A. L., & Raggio, D. P. (2012). Parental reports of the oral health-related quality of life of children with cerebral palsy. BMC Oral Health, 12, 15. doi:10.1186/1472-6831-12-15

Aguilar-Díaz, F. C., Irigoyen-Camacho, M. E., & Borges-Yáñez, S. A. (2011). Oral-health-related quality of life in schoolchildren in an endemic fluorosis area of Mexico. Quality of Life Research : An International Journal of Quality of Life Aspects of Treatment, Care and Rehabilitation, 20(10), 1699–706.

Chikte, U. M., Louw, A. J., & Stander, I. (2001). Perceptions of fluorosis in northern Cape communities. SADJ : Journal of the South African Dental Association = Tydskrif van Die Suid-Afrikaanse Tandheelkundige Vereniging, 56(11), 528–32.

Choi, A. L., Sun, G., Zhang, Y., & Grandjean, P. (2012). Developmental fluoride neurotoxicity: A systematic review and meta-analysis. Environmental Health Perspectives, 120(10), 1362–1368.

Choi, A. L., Zhang, Y., Sun, G., Bellinger, D., Wang, K., Yang, X. J., … Grandjean, P. (2015). Association of lifetime exposure to fluoride and cognitive functions in Chinese children: A pilot study. Neurotoxicology and Teratology, 47, 96–101.

Cunnion, D. T., Spiro, A., Jones, J. a, Rich, S. E., Papageorgiou, C. P., Tate, A., … Garcia, R. I. (2010). Pediatric oral health-related quality of life improvement after treatment of early childhood caries: a prospective multisite study. Journal of Dentistry for Children, 77, 4–11.

Do, L. G., & Spencer, A. (2007). Oral Health-Related Quality of Life of Children by Dental Caries and Fluorosis Experience. Journal of Public Health Dentistry, 67(3), 132–139.

Kramer, P. F., Feldens, C. A., Ferreira, S. H., Bervian, J., Rodrigues, P. H., & Peres, M. A. (2013). Exploring the impact of oral diseases and disorders on quality of life of preschool children. Community Dentistry and Oral Epidemiology, 41(4), 327–35.

NZ Ministry of Health. (2010). Our Oral Health Key findings of the 2009 New Zealand Oral Health Survey.

Perrott, K. W. (2015). Severe dental fluorosis and cognitive deficits. Neurotoxicology and Teratology.

Scarpelli, A. C., Paiva, S. M., Viegas, C. M., Carvalho, A. C., Ferreira, F. M., & Pordeus, I. A. (2013). Oral health-related quality of life among Brazilian preschool children. Community Dentistry and Oral Epidemiology, 41(4), 336–44.

NZ Fluoridation review – HS Micklen responds to critique

I have posted several articles in a series critiquing contributions to the Fluoride Free NZ report Scientific and Critical Analysis of the 2014 New Zealand Fluoridation Report which is aimed at discrediting the recent review Health Effects of Water Fluoridation: a Review of the Scientific Evidence produced by the Royal Society of NZ together with the Office of the Prime Minister’s Chief Science Advisor. The articles in this series are collected into a pdf document which can be downloads from Download report analysing anti-fluoride attacks on NZ Fluoridation Review.

In an attempt to encourage a discussion on the fluoridation review and the FFNZ report I offered all the authors and “peer-reviewers” of the FFNZ report the right of reply to my critiques. So far Dr H. S. Micklen (whose article I critiqued in Fluoride Free NZ report disingenuous – conclusion), is the only one to take up this offer.

Here is his reply. 


I thank Dr Perrott for reproducing my notes on the NZ Fluoridation Review and appreciate his comments. My appreciation would be warmer had he spent less time using his imagination and paid more attention to what I actually wrote.  He has me bustling around, agenda in hand, clutching at straws here, raising bogeys there, scaremongering, relying on this, calling for that, and getting confused about different grades of fluorosis (as if..,). All nonsense.  If I “distort the science” as Perrott’s headline proclaims, he does a great job of distorting the distortion.

Most of my short piece merely commented on a few places where, in my opinion, the NZ report failed – through error, omission or incompetence – to reach proper standards of objectivity and impartiality and exhibited ill-founded complacency. Since the NZ report was highly biased in favour of fluoridation, any criticisms of it are likely to have an anti-F flavour. Too bad; I was dealing with the report’s view of the science, not pushing my own. I avoided speculating on the outcome of issues that I consider unresolved, dental fluorosis (where Perrott makes nonsense of what I wrote) being the only exception.

Most of these issues have been argued over ad nauseam and I shall not try to unscramble Perrott’s lucubrations. The question of chronic kidney disease and its possible cardiovascular consequences is perhaps an exception. I gave credit to the Review for discussing the paper by Martin-Pardillos. Agreeing with the Review’s opinion that the results needed to be confirmed, I remarked “The interesting question is, what should happen meanwhile?” That is not a rhetorical question. What does, or should, happen when an alarm bell sounds over a long-established procedure? Does further research on the topic receive any funding priority, for example?  Perrott uses a piece of grammatical legerdemain to pretend that I called for CKD sufferers to be warned to avoid tap water, which I did not. In fact, I am inclined to agree with him that that might be extreme in the present state of knowledge. Perhaps it would be embarrassing, too, for a government to insist on putting fluoride in the water and then advise a substantial number of people not to drink it – or so one might think. But Perrott concludes “Any patients who are particularly worried can then take steps like using filtered water for their own peace of mind. This seems more appropriate than denying the rest of the population access to a simple, effective and safe (for them at least) social health policy like CWF.”  So that’s all right then, thanks to the patients, whom Perrott doubtless consulted, being willing to promote the alleged greater good. He has pricked a hole in the old mantra, though: “effective and safe – for some”.

Perrott asked for my feedback on his idea about the possible effect of dental fluorosis on IQ.  Since then his paper has appeared online as a short article in Neurotoxicology and Teratology. Perhaps the best thing I can do at this stage is pretend that it had arrived on my desk for peer review. I would have commented as follows.

“This communication refers to a recent paper by Choi et al (2014) that reports certain cognitive defects in young children affected by moderate-severe dental fluorosis. Choi et al suggest that this is due to an adverse effect of fluoride on the developing brain. The present author proposes an alternative explanation, namely that fluorosis itself, and the stress of living with it, can affect learning and general quality of life and result in poor performance in certain types of cognitive test. This appears to be a novel idea and, as such, is suitable in principle for publication as a short communication. There is, however, a fundamental question that the author should be invited to address and clarify with a view to possible resubmission.

“The paper is somewhat discursive and lacking in focus and in the course of it the author seems to lose track of what age group he is talking about. Surprisingly, he does not mention the age of Choi’s (2014) subjects, which averaged 7 years  (range 6-8). When he finally presents evidence that moderate-severe fluorosis is aesthetically displeasing and likely to impair quality of life, all of it relates to older children, mainly teenagers, who have reached an age to be self-conscious about their appearance and have been living with fluorosis for several years. In contrast, 16% of Choi’s (2014) subjects had no erupted permanent teeth at all and in the remainder eruption of the first permanent teeth would have been very recent. Since fluorosis was common in the community, having the condition would not appear abnormal. The crucial question is whether the author is proposing that the quality of life of these young children is so compromised by fluorosis as to impair their performance in cognitive tests. Apparently the answer is a tentative affirmative: It is just possible that the negative quality of life associated with oral defects like severe dental fluorosis contribute to cognitive deficits reported by Choi et al. (2012, 2014)’

“The author needs to discuss this issue in a transparent fashion so that readers can judge for themselves whether the proposal is plausible. Conversely, if he is not making such a proposal, that too should be made clear.

“The author might wish to refresh his memory of the paper by Hilsheimer and Kurko (1979), which really is of virtually no relevance to his argument.”

I hope this helps.

H S M 12 February 2015

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