Ashley Malin - A New Fluoride Expert?
When the NTP released its deeply flawed report on fluoride neurotoxicity, it received widespread media attention. Many outlets carried the story through the Associated Press, including commentary from Ashley Malin, a former member of Christine Till’s team at York University and now an Assistant Professor at the University of Florida. Echoing claims made by the Fluoride Action Network, Malin described the report as “the most rigorously conducted of its kind.”
As PFPC members know, nothing could be further from the truth.
Malin has been the lead author of numerous studies on fluoride and neurotoxicity, all of which demonstrate a concerning lack of understanding regarding the interaction between fluoride and iodine. Her consistent misinterpretation of the literature is also a hallmark of the Till team's publications on fluoride effects.
Here, we examine one of her most widely cited papers, also included in the recent NTP report, titled "Fluoride exposure and thyroid function among adults living in Canada: Effect modification by iodine status." (Malin et al, 2018)
We will explore some of the significant gaps in Malin's understanding of the subject.
1. IODINE STATUS
When the title of a study includes the phrase "Effect modification by iodine status," one naturally expects the research to thoroughly address iodine status and how various iodine states in a population are defined in the global literature. Organizations like the WHO and the International Council for Iodine Deficiency Disorders have long established guidelines and categories that define the different stages of iodine sufficiency.
The World Health Organization (WHO) provides the following definitions and categories for iodine status based on urinary iodine concentration (UIC) in general populations (not pregnancy):
- Severe Iodine Deficiency: UIC < 20 µg/L
- Moderate Iodine Deficiency: UIC 20-49 µg/L
- Mild Iodine Deficiency: UIC 50-99 µg/L
- Adequate Iodine Nutrition: UIC 100-199 µg/L
- More-than-Adequate Iodine Nutrition: UIC 200-299 µg/L
- Excessive Iodine Intake: UIC ≥ 300 µg/L
Malin et al, however, as did other Till team members in later studies, used their own definition of "adequate" or sufficient status - all the while claiming they were relying on WHO guidelines from a 2004 document:
Converted to µg/L (micrograms per liter) - the standard unit used in most guideline and studies - that would be >48.22 μg/L and ≤300.75 μg/L."Moderate-to-severe iodine deficiency was defined as urinary iodine ≤0.38 μmol/L using guidelines established by the World Health Organization (Iodine Status Worldwide: WHO Global Database on Iodine Deficiency, 2004). Participants were considered to have adequate levels of iodine if the urinary iodine value fell between >0.38 and ≤2.37 μmol/L."
This means that Malin’s “adequate” range, supposedly based on WHO guidelines, actually combined three distinct WHO categories: mildly deficient iodine intake (UIC 50-99 µg/L), adequate iodine intake (UIC 100-199 µg/L), and more-than-adequate iodine intake (UIC 200-299 µg/L). In other words, the so-called “adequate” group was not an adequate-iodine group at all.
- NOTE: Urinary iodine concentration (UIC) is commonly stated in µg/L (micrograms per liter). This is the standard unit used in most guidelines and studies, including those by the World Health Organization (WHO) and other health organizations. Using µg/L allows for direct comparison with established reference ranges for iodine status in populations.
This mistake in defining "adequate" iodine status would have significant implications for the study's findings and conclusions. Here’s how it could impact the study:
Misclassification of Iodine Status:
By including both mildly deficient and more-than-adequate iodine levels in the same "adequate" category, the study misclassifies participants' iodine status. This blurs the distinction between different iodine states, which are known to have different effects on thyroid function and overall health.
Diluted Findings:
The potential health effects associated with true iodine sufficiency (UIC 100-199 µg/L) could be diluted by the inclusion of individuals with mild deficiency (UIC 50-99 µg/L) or more-than-adequate iodine intake (UIC 200-299 µg/L). This could lead to inaccurate associations or weaken the observed effects between fluoride exposure and thyroid function.
Confounding Effects:
Different iodine levels interact with fluoride in different ways. For example, mild iodine deficiency might exacerbate the effects of fluoride on thyroid function, while excessive iodine might have its own set of complications. By not properly categorizing these levels, the study could attribute effects to fluoride that are actually due to the varying iodine statuses of the participants.
Faulty Conclusions:
The study’s conclusions about the relationship between fluoride exposure and thyroid function could be flawed. If participants are not accurately grouped by iodine status, the observed effects might not be representative of the actual impact of fluoride, leading to potentially misleading public health recommendations.
Inaccurate Public Health Implications:
If policymakers or health professionals rely on the study's findings, they might implement recommendations that are not properly tailored to the actual risks. This could result in either underestimating the risks of fluoride exposure in certain populations or overestimating them, depending on the specific iodine status misclassifications.
Undermining of Research Credibility:
Such a fundamental error in defining key variables undermines the credibility of the research and the trustworthiness of its findings. This mistake compromises the study's internal validity, leading to potentially incorrect conclusions about the interaction between fluoride and iodine and their combined effects on thyroid health.
2. SAMPLE COLLECTION
In Malin's study, fluoride exposure was assessed using spot urine samples that were not standardized with respect to the time of collection. Similarly, the timing of blood collection for TSH tests was not standardized.
Because fluoride was measured from spot urine samples collected at varying times, the results may not accurately reflect consistent fluoride exposure levels due to the compound's short half-life and fluctuations in daily behaviors. This inconsistency in sample collection times could lead to a misclassification of exposure levels. The authors suggest that this misclassification should be non-differential, meaning it would affect all groups equally, likely resulting in a bias toward underestimating the true effect (bias toward the null).
However, this assumption is not established.
TSH levels follow a normal circadian rhythm, peaking mid-day and reaching their lowest levels between 5 pm and 8 pm. Additionally, TSH secretion is characterized by secretory pulses every 2-3 hours, interspersed with periods of nonpulsatile secretion. This variation in TSH levels throughout the day means that if TSH measurements are taken at different times without standardization, the results could be highly variable and may not accurately reflect the true thyroid status. This variability could potentially lead to misleading conclusions in studies involving TSH measurements.
If these variations are not accounted for, the study may inaccurately capture the relationship between fluoride and TSH. This could lead to either overestimating or underestimating the true effects, rather than simply biasing the results toward the null.
3. MISREPRESENTATION OF THE SCIENTIFIC LITERATURE
Misrepresenting and misunderstanding the scientific literature on the effects of fluoride on iodine/thyroid hormone metabolism has been a hallmark of the York/MIREC studies. Similarly, the study by Malin et al. exhibits comparable issues. Three examples shall be given here:
A) Zhao et al. (1998)
Malin et al., wrote:
Firstly, Zhao's study was on mice, not rats. Secondly, the findings are not quite as reported by Malin et al."Prevalence of dental fluorosis and bone fluoride concentrations have also been shown to be significantly higher among rats with iodine deficiencies than rats with normal or excess iodine levels [emphasis added], despite both having equivalent excess fluoride concentration exposures (Zhao et al., 1998)."
When considering the incidence (rate) of dental fluorosis across all observation times:
ID = Iodine Deficiency
IE = Iodine Excess
FD = Fluoride Deficiency
FE = Fluoride Excess
- Day 30: The ID+FE group had the highest incidence at 92.9%.
- Day 60: Both the ID+FE and IE+FE groups showed 100% incidence.
- Day 90: The ID+FE group maintained 100% incidence, while the IE+FE group had 86.7%.
- Day 150: Both the ID+FE and IN+FE groups showed 100% incidence.
B) Xu & Zhang, 1994 & Zhao et al., 1998
Malin et al., wrote:
There is no evidence/excretion data at all in the papers by Xu et al. (1994) or Zhao et al. (1998) to justify this statement."There is also evidence that despite fluoride's lighter atomic weight, iodine may contribute to increased excretion of fluoride from the body (Xu & Zhang, 1994; Zhao et al., 1998)."
While there are certainly studies showing the mutual interacting effects of iodine and fluoride in urine excretion, these studies listed by Malin do not qualify as "evidence".
C) Xu & Zhang, 1994 & Zhao et al. 1998
Malin et al., wrote:
This is an incorrect assumption. Fluoride will exacerbate the effects of iodine deficiency. Malin conveniently forgot to mention that "excess" fluoride reduces goiter caused by excessive iodine - the very reason why fluoride was used in the treatment of iodine-induced hyperthyroidism.Adequate iodine levels can offset adverse goitrogenic effects of fluoride (Xu & Zhang, 1994; Zhao et al., 1998).
Zhao's observations (Table 3) suggest that excess iodine has a more pronounced effect on thyroid enlargement (goiter) than excess fluoride, especially when iodine is present in excess. This aligns with the understanding that while fluoride can contribute to goiter under certain conditions, iodine levels, particularly excess or deficient iodine, play a crucial role in thyroid health and can lead to more significant thyroid enlargement/dysfunction than fluoride might.
Xu et al. also show that with similar iodine levels, an increase in fluoride concentration from 0.5 mg/L to 0.8 mg/L is associated with a decrease in the goiter rate from 45.0% to 10.6%.
Higher fluoride levels (3.9 mg/L) in combination with moderate to high iodine levels (670 pg/L) show a relatively low goiter rate (11.22%), compared to lower fluoride levels (0.5 mg/L) with high iodine concentrations (10,000 pg/L), which shows a higher goiter rate (22.4%).
4. SAMPLE GROUP
Malin et al. limited their analyses to adults aged 18 and over, citing "the low prevalence of hypothyroidism in younger individuals" as the rationale.
This decision highlights a significant gap in their understanding of iodine-related thyroid disorders. The authors appear to assume that iodine issues are solely linked to iodine deficiency and its role in causing hypothyroidism. While iodine deficiency can indeed lead to hypothyroidism, it can also cause hyperthyroidism. Moreover, more-than-adequate and excessive iodine intake is associated with both subclinical and clinical hypothyroidism, as well as hyperthyroidism. In fact, high iodine consumption is a primary cause of subclinical hypothyroidism in pregnant women (Candido et al., 2023).
If the authors were genuinely concerned about the potential modifying effects of iodine status on fluoride's impact on thyroid function, they should have included data from all age groups, especially children. This is particularly relevant given that the Cycle 3 survey revealed that the majority of children aged 3 to 5 years had more-than-adequate iodine intake, with 40% having excessive levels. This is the same age group that was studied for fluoride's effect on IQ by Till and her team at York University (Green et al., 2019). Recent studies have also shown that a urinary iodine concentration (UIC) indicative of more-than-adequate (200-299 µg/L) and excessive iodine intake (>300 µg/L) is associated with a loss of IQ (Cui et al., 2020; Kampouri et al., 2024).
Additionally, TSH levels can vary significantly with age, gender (especially during puberty), and conditions such as diabetes. The impact on T3/T4 ratios - a common disturbance observed in fluoride poisoning - also changes after the age of 40 (Strich et al., 2016). Had Malin et al. fully considered this variability, they might have focused on the most stable age group (20 to 39 years), where TSH levels are generally more consistent.
Instead, their sample had a mean (SD) age of 46.5 (15.6) years, offering only limited insight into how age-related changes in thyroid function could interact with fluoride exposure.
The exclusion of younger individuals, particularly children who are at higher risk of both iodine excess and deficiency, further limits the study's applicability. Given that the critical developmental period for thyroid function and cognitive development occurs in early childhood, this demographic is essential when examining the impacts of fluoride exposure and iodine status. The failure to do so raises questions about the robustness of the study’s conclusions and whether they can be generalized across different age groups and iodine status categories.
In summary, by excluding younger individuals and not accounting for the variability in TSH levels across different ages, Malin et al. may have overlooked key factors that could modify the relationship between fluoride exposure and thyroid function. These limitations, along with the misclassification of iodine status, suggest that the study's findings may not fully capture the complexities of this interaction, ultimately limiting the accuracy and relevance of its conclusions.
Wendy Small
PFPC Canada
REFERENCES:
Candido AC, Vieira AA, de Souza Ferreira E, Moreira TR, do Carmo Castro Franceschini S, Cotta RMM - "Prevalence of Excessive Iodine Intake in Pregnancy and Its Health Consequences: Systematic Review and Meta-analysis" Biol Trace Elem Res 201(6):2784-2794 (2023) doi: 10.1007/s12011-022-03401-5
https://link.springer.com/article/10.10 ... 22-03401-5
"The prevalence of excessive iodine intake in 10,736 pregnant women in different regions of the world was 52%...the farther the trimester of gestation and the lower the FT4, the higher the prevalence of iodine excess. The main implications for pregnant women were hypothyroxinemia, hypothyroidism, and hyperthyroidism. For the newborn, macrosomia and thyroid dysfunction."
Green R, Lanphear B, Hornung R, Flora D, Martinez-Mier EA, Neufeld R, Ayotte P, Muckle G, Till C - "Association Between Maternal Fluoride Exposure During Pregnancy and IQ Scores in Offspring in Canada" JAMA Pediatr 173(10):940-948 (2019) doi: 10.1001/jamapediatrics.2019.1729 MIREC
https://jamanetwork.com/journals/jamape ... le/2748634
Kampouri M, Margetaki K, Koutra K, Kyriklaki A, Daraki V, Roumeliotaki T, Bempi V, Vafeiadi M, Kogevinas M, Chatzi L, Kippler M - "Urinary iodine concentrations in preschoolers and cognitive development at 4 and 6 years of age, the Rhea mother-child cohort on Crete, Greece" J Trace Elem Med Biol 85:127486 (2024). doi: 10.1016/j.jtemb.2024.127486 RHEA
https://linkinghub.elsevier.com/retriev ... 24)00106-8
"Children with UIC ≥300 μg/L had lower cognitive scores both at 4 (MSCA; B= -3.5; 95 %CI -6.9, -0.1; n =101) and 6 years of age (RCPM-total score; B= -1.2; 95 %CI -2.3, -0.0; n =98) than children in the reference group."
NOTE: UICs above 181 μg/L showed downward cognition scores.
Malin AJ, Riddell J, McCague H, Till C - "Fluoride exposure and thyroid function among adults living in Canada: Effect
modification by iodine status" Environ Int 121(Pt 1):667-674 (2018)
doi: 10.1016/j.envint.2018.09.026.
https://www.sciencedirect.com/science/a ... 201830833X
Strich D, Karavani G, Edri S, Gillis D. - "TSH enhancement of FT4 to FT3 conversion is age dependent" Eur J Endocrinol 175(1):49-54 (2016)
https://pubmed.ncbi.nlm.nih.gov/27150496/
https://eje.bioscientifica.com/view/jou ... 5/1/49.xml
"As TSH levels increase, FT3/FT4 ratios increase until age 40, but this differential increase does not occur in older age groups."
Teng X, Shan Z, Chen Y, Lai Y, Yu J, Shan L, Bai X, Li Y, Li N, Li Z, Wang S, Xing Q, Xue H, Zhu L, Hou X, Fan C, Teng W - "More than adequate iodine intake may increase subclinical hypothyroidism and autoimmune thyroiditis: a cross-sectional study based on two Chinese communities with different iodine intake levels" European Journal of Endocrinology 164(6):943-950 (2011)
https://doi.org/10.1530/EJE-10-1041
"More than adequate iodine intake could be a public health concern in terms of thyroid function and thyroid autoimmunity in the Chinese populations."
The data supporting the point are that Rongxing had MUI 261 µg/L, while Chengshan had MUI 145 µg/L, and the prevalence of subclinical hypothyroidism was higher in Rongxing: 5.03% vs 1.99%. TPOAb positivity was also higher: 10.64% vs 8.4%, and TgAb positivity was higher: 10.27% vs 7.93%.
Teng W, Shan Z, Teng X, Guan H, Li Y, Teng D, Jin Y, Yu X, Fan C, Chong W, Yang F, Dai H, Yu Y, Li J, Chen Y, Zhao D, Shi X, Hu F, Mao J, Gu X, Yang R, Tong Y, Wang W, Gao T, Li C - "Effect of iodine intake on thyroid diseases in China" New England Journal of Medicine 354(26):2783-2793 (2006)
https://doi.org/10.1056/NEJMoa054022
"More than adequate or excessive iodine intake may lead to hypothyroidism and autoimmune thyroiditis."
WHO - Iodine Status Worldwide: WHO Global Database on Iodine Deficiency (2004)
https://www.who.int/publications/i/item/9241592001
Xu Y, Lu C, Zhang X - "The Effect of Fluoride on the Level of Intelligence in Children" Endemic Diseases Bulletin 9(2):83-84 (1994)
https://www.fluoridealert.org/wp-conten ... u-1994.pdf
Zhao W, Zhu H, Yu Z, Aoki K, Misumi J, Zhang X - "Long-term Effects of Various Iodine and Fluorine Doses on the Thyroid and Fluorosis in Mice" Endocr Regul 32 (2):63-70 (1998)
https://poisonfluoride.com/dir/wp-conte ... o-1998.pdf
Further comments by PFPC Members:
- Malin et al. excluded people with reported thyroid conditions or thyroid medication use.
- Excluded people with excess iodine - that makes the paper narrower than its title suggests.
- The paper reports that iodine-deficient adults had lower tap-water fluoride concentrations than non-deficient adults, but higher arithmetic mean urinary fluoride. The geometric means were identical, and medians were similar. That complicates the interpretation. It shows that urinary fluoride differences may reflect tea, diet, recent intake, renal handling, hydration, or sampling variability rather than community water fluoridation exposure.
- Malin et al. present Na,K-ATPase inhibition as a thyroid-relevant mechanism, but the cited Na,K-ATPase studies are not thyroid studies. They support a general biochemical effect of fluoride on ATPase activity, not direct evidence that fluoride disrupts thyroidal iodide uptake through Na,K-ATPase or NIS in human thyroid tissue.
- Malin et al. limited their analysis to adults aged 18 and older, citing “the low prevalence of hypothyroidism in younger individuals” as the rationale. This justification is too narrow. The study was framed as an analysis of effect modification by iodine status, not merely as a study of diagnosed hypothyroidism. If iodine status was central to the analysis, then younger age groups should not have been dismissed simply "because overt hypothyroidism is less common". This is especially important because CHMS Cycle 3 showed that the majority of children aged 3 to 5 years had more-than-adequate iodine intake, with 40% having excessive iodine intake.
- They excluded participants with excess iodine and then treated everyone from just above moderate-to-severe deficiency up to the threshold for excess as “adequate.” As a result, the analysis was not really iodine-status effect modification. It was a comparison between moderate-to-severe iodine deficiency and a mixed non-deficient group that included mild deficiency, adequate iodine intake, and more-than-adequate iodine intake.
- Malin et al. adjusted for age and sex as separate covariates, but this does not fully account for sex-specific age effects on TSH. Because TSH changes with age differently in women and men, age and sex should not simply be treated as independent covariates. At minimum, the model should have tested an age-by-sex interaction or presented sex-stratified age analyses. This is especially important because the supplement shows that urinary fluoride levels also varied by both age and sex, with older females having the highest mean UFSG.
- Malin et al. treated iodine status as a binary variable based on uncorrected spot UIC, while correcting urinary fluoride for specific gravity and, in supplemental analyses, creatinine. They did not define iodine status using UIC/Cr or UIC/SG, even though corrected iodine measures can differ substantially by sex and age.
See PFPC table for 20-39 age group from Cycle 3: https://poisonfluoride.com/Science/NTP_ ... _data.html