You may not be aware but the ARTICLE OF THE YEAR in 2019 in the world’s premier Paediatrics journal, JAMA Pediatrics, was a study by Green et al which found an association between prenatal fluoride exposure in pregnancy and lower IQ in offspring. This study by a team of researchers from numerous universities from Canada and the United States was conducted in communities across Canada and examined for the very first time fluoride intake among pregnant mothers in fluoridated and non-fluoridated communities in North America and its effects on the IQ of offspring. Importantly, this study confirms the findings of previous studies published in Central America and China.

The study authors included previous research from Ireland addressing largely undocumented and uncontrolled exposures to fluoride from other dietary sources apart from water through the consumption of tea. As noted previously by Waugh et al in their study titled “Risk Assessment of Fluoride intake from Tea in the Republic of Ireland and its implications for Public Health and Water Fluoridation” the habitual consumption of tea in addition to consumption of fluoridated water can result in excessive fluoride intake and may contribute to a wide range of diverse negative health outcomes including thyroid disorders, cardiovascular system dysfunctions and musculoskeletal disorders.
This seminal study by Waugh et al directly questioned the lack of rigour and risk assessment of fluoride intake by the Department of Health among the population in Ireland where the majority of the adult population drink tea. Ironically, public health authorities have known since the late 1930s that tea is a major source of fluoride, yet despite Ireland having the highest per capita consumption of the tea in the world for almost a century and introducing mandatory fluoridation of water in the 1960s nobody prior to this study being published had measured the fluoride content in teas available in Ireland.

The JAMA Pediatrics study acknowledged, using this published research as evidence, that one cannot account for fluoride intake alone based on water consumption and that one must include other sources such as tea, when determining population or individual level exposure to this toxin. However, it is also notable, that the JAMA study in question on infant IQ, observed a highly significant finding. In particular, they found a sex specific relationship between maternal intake in pregnancy and lower IQ in offspring which affected male offspring more than females. While it has long been acknowledged that the male sex is more susceptible to neuro-developmental brain disorders than females, the biological or molecular mechanisms that may contribute to this sex specificity have remained elusive to date.

This observation of sex specificity was discussed in some detail by the editors of JAMA Pediatrics in their Podcast supporting the journals justification for publishing the Green et al study. Interestingly, while the journal editors acknowledged that sex specificity of brain disorders are well documented for boys versus girls they also acknowledged that the underlying basis for these observations remains largely unknown. Remarkably, in response to this podcast and the Green et al study Waugh wrote to the editors of the journal presenting for the first time a coherent and biologically plausible mechanistic reason why males are more susceptible to chemical induced neurodevelopmental disorders than females, which would explain the findings of this seminal study, as well as other studies showing higher prevalence of brain disorders among males from prenatal chemical exposure to toxins. Following peer review this explanation was published in JAMA Pediatrics on the 30th December 2019. In this, Waugh explains several reasons why the male sex is more susceptible to prenatal chemical exposures that may result in increased susceptibility to neurodevelopmental disorders among boys versus girls. In summary, four points were addressed.
Firstly, Waugh explains that the female sex has a genetic advantage compared to males in coping with chemical toxicity owing to sex specific differences in total antioxidant status and the genetic expression of enzymes involved in mitigating oxidative stress and inflammatory signalling.
Secondly, Waugh addresses how mothers of female offspring have lower levels of reactive oxygen species associated with oxidative stress & higher total antioxidant status than mothers of boys, indicating that mothers of male infants are more susceptible to chemical insult during pregnancy.
Next, Waugh identifies how scientific studies have shown that mitochondria from female individuals are more resistant to the effects of oxidative stress induced by fluoride or other chemical intoxication. Finally, Waugh addresses how in vivo experimental studies have shown that prenatal and perinatal exposure to fluoride induces mitochondrial dysfunction in the developing central nervous system and that mitochondrial disruption in turn induces neurodevelopmental disorders. Taken together, these novel insights by Waugh are invaluable. They identify not just the knowledge gaps, but where research in environmental toxicology needs to be directed in future to address the adverse effects of prenatal chemical exposures and the growing burden of neurodevelopmental disorders in children today.

It is worthy of interest that the contribution by Waugh to environmental toxicology is also being noticed by leading experts in this scientific discipline. Most recently, Professor Philippe Grandjean, of Harvard School of Public Health published an updated Review on, Developmental Fluoride Neurotoxicity which was published last month in the internationally renowned journal Environmental Health. In this seminal publication, Grandjean also references another study by Waugh et al which examined the health risks of fluoride intake among the population in New Zealand.

Moreover, Waugh recently published three major reviews in peer reviewed scientific literature which contribute significantly to the gap in knowledge in understanding the molecular mechanisms of action of fluoride toxicity and which highlight how exposure to fluoride may contribute to a diverse range of adverse health effects including eye diseases, iodine deficiency and inhibition of a crucial enzyme called Sodium-and Potassium-Activated Adenosine Triphosphatase (also called Na+, K+-ATPase or NKA). Most importantly, inhibition of NKA has been implicated in the pathogenesis of a vast number of diseases including, cancer progression, pulmonary disorders, metabolic disorders as well as neuro-developmental, neuropsychiatric and neurodegenerative disorders…


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