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• Response to Barberio et al's claim that there is no link between fluoridation and hypothyroidism
  Stephen Peckham, David Lowery and Sarah Spencer
  Published on: 24 January 2018

• Published on: 24 January 2018

  Response to Barberio et al's claim that there is no link between fluoridation and hypothyroidism

  • Stephen Peckham, Professor of Health policy Centre for Health Services Studies, University of Kent
  • Other Contributors:
    • David Lowery, Research Fellow
    • Sarah Spencer, Research associate

  Barberio et al1 report a study which – in contrast to our own study2 - shows no relationship between fluoride intake and hypothyroidism. However, Barberio et al study is limited by the methods used for identifying hypothyroidism prevalence, fluoridation status and sample sizes.

  Barberio et al utilised three methods to determine hypothyroidism prevalence: self-report and two biomarkers: thyroid-stimulating hormone (TSH), and free T4 blood results. This is problematic as self-report is unlikely to provide accurate prevalence data when compared to clinical diagnosis data, as used in our study4; and there are a number of studies demonstrating that self-reported estimates of thyroid functioning are unreliable. Further, the self-report question does not appear to differentiate between under and over active thyroid functioning. The biomarker data only included individuals with un-medicated hypothyroidism; consequently, the sample is unrepresentative of the population. The analysis of this data provides correlations between the biomarkers TSH, T4 readings and fluoride exposure in a sub-sample of respondents, assuming that all respondents received uniform levels of fluoride. From our data, we observed wide variability within fluoridated areas. This may explain why in table 2b, none of the variables, including age and sex, were predictive of TSH levels. This contradicts Barberio et al’s own data on what is predictive of hypothyroidism and the Canadian Health Measures Survey...

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  Barberio et al1 report a study which – in contrast to our own study2 - shows no relationship between fluoride intake and hypothyroidism. However, Barberio et al study is limited by the methods used for identifying hypothyroidism prevalence, fluoridation status and sample sizes.

  Barberio et al utilised three methods to determine hypothyroidism prevalence: self-report and two biomarkers: thyroid-stimulating hormone (TSH), and free T4 blood results. This is problematic as self-report is unlikely to provide accurate prevalence data when compared to clinical diagnosis data, as used in our study4; and there are a number of studies demonstrating that self-reported estimates of thyroid functioning are unreliable. Further, the self-report question does not appear to differentiate between under and over active thyroid functioning. The biomarker data only included individuals with un-medicated hypothyroidism; consequently, the sample is unrepresentative of the population. The analysis of this data provides correlations between the biomarkers TSH, T4 readings and fluoride exposure in a sub-sample of respondents, assuming that all respondents received uniform levels of fluoride. From our data, we observed wide variability within fluoridated areas. This may explain why in table 2b, none of the variables, including age and sex, were predictive of TSH levels. This contradicts Barberio et al’s own data on what is predictive of hypothyroidism and the Canadian Health Measures Survey prevalence estimates for hypothyroidism. 3 Finally, The sample size for the individual level fluoride status was much smaller that the full sample and not reported fully within the paper; indeed, Statistics Canada prohibited the authors from carrying out some analyses due to ‘sample sizes requirements’. It is reasonable to estimate that no more than 15 people with hypothyroidism are likely to be included in the sample reported in table 3; this raises questions about the statistical power of this analysis.

  Barberio et al suggest that the differences in findings could be – in part - due to iodine deficiency in England; however, they did not refer to the most recent data which showed that iodine intake was adequate in all age/sex groups.5 We suggest that the different classification of hypothyroidism prevalence and potential weaknesses in the statistical analysis account for the different findings of the two studies. We believe the following questions need to be answered:

  1. How certain are they that participants understood they were being asked specifically about hypothyroidism when asked if they had a ‘thyroid condition’?

  2. Why do they think age and sex, which are uncontentious predictors of hypothyroidism, do not provide any predictive value in the model of the biomarker TSH (presented in Table 2b)?

  3. What was the statistical power for the comparisons presented in tables 3a and b?

  Without further clarification of these issues, it is not possible to have confidence in the findings reported by Barberio et al, and we do not accept that their study refutes our findings. However, we do agree with Barberio et al and other commentators that more individual level analyses are required to explore the relationship between thyroid function and fluoride exposure.

  References:

  1. Barberio AM, Hosein FS, Quiñonez C, McLaren L. Fluoride exposure and indicators of thyroid functioning in the Canadian population: implications for community water fluoridation. J Epidemiol Community Health. 2017 Oct 1;71(10):1019-25.

  2. Peckham S, Lowery D, Spencer S. 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 2015;69:619–24.

  3. Rotermann, M., Sanmartin, C., Hennessy, D., & Arthur, M. (2014). Prescription medication use by Canadians aged 6 to 79. Health reports, 25(6), 3.

  4. Banks E, Beral V, Cameron R, Hogg A, Langley N, Barnes I, Bull D, Elliman J, Harris CL. Agreement between general practice prescription data and self-reported use of hormone replacement therapy and treatment for various illnesses. Journal of Epidemiology and Biostatistics. 2001 Jul 1;6(4):357-63.

  5. National Diet and Nutrition Survey results from years 5 and 6 (combined) of the rolling programme (2012/2013–2013/2014), Public Health England, London (2016) https://www.gov.uk/government/uploads/system/uploads/attachment_data/fil...

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  Conflict of Interest:
  None declared.

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