Benoit Follin-Arbelet, Bjørn Moum. Fluoride: A Risk Factor for Inflammatory Bowel Disease? Scand J Gastroenterol, 51 (9), 1019-24, Sep 2016
Although the association between inflammatory bowel disease (IBD) and oral hygiene has been noticed before, there has been little research on prolonged fluoride exposure as a possible risk factor. In the presented cases, exposure to fluoride seems indirectly associated with higher incidence of IBD. Fluoride toxicology and epidemiology documents frequent unspecific chronic gastrointestinal symptoms and intestinal inflammation. Efflux genes that confer resistance to environmental fluoride may select for IBD associated gut microbiota and therefore be involved in the pathogenesis. Together these multidisciplinary results argue for further investigation on the hypothesis of fluoride as a risk factor for IBD.
“The illness appears to be less severe outside China, but a new study reports that this virus often looks benign to start with. It begins with a mix of mild symptoms that can look like the common cold, or resemble gastro. But some patients go on to develop breathing trouble five days later, and may need the ICU (Intensive Care Unit) by day 8. Sometimes people get released from medical care, but then have to return the next week. So not only must we wait 14 days for the incubation period, there may be another 8 days (or more) before we know how many will need emergency life support and we can begin to calculate the fatality rate.” click here
“A horrific though unverified video has leaked out of China, allegedly from a hospital in Wuhan, showing dead bodies laying in a corridor unattended, with sick people sitting next to them waiting for treatment.” click here
“According to the American Cancer Society, “the largest single-year drop ever recorded” for cancer deaths in America took place from 2016-17 in the amount of a 2.2 percentage point decrease. This is the most recent time period that data is available.” click here
Waugh DT. Fluoride Exposure Induces Inhibition of Sodium/Iodide Symporter (NIS) Contributing to Impaired Iodine Absorption and Iodine Deficiency: Molecular Mechanisms of Inhibition and Implications for Public Health. Int J Environ Res Public Health. 2019 Mar 26;16(6). pii: E1086. doi: 10.3390/ijerph16061086.
The sodium iodide symporter (NIS) is the plasma membrane glycoprotein that mediates active iodide transport in the thyroid and other tissues, such as the salivary, gastric mucosa, rectal mucosa, bronchial mucosa, placenta and mammary glands. In the thyroid, NIS mediates the uptake and accumulation of iodine and its activity is crucial for the development of the central nervous system and disease prevention. Since the discovery of NIS in 1996, research has further shown that NIS functionality and iodine transport is dependent on the activity of the sodium potassium activated adenosine 5′-triphosphatase pump (Na+, K+-ATPase). In this article, I review the molecular mechanisms by which F inhibits NIS expression and functionality which in turn contributes to impaired iodide absorption, diminished iodide-concentrating ability and iodine deficiency disorders. I discuss how NIS expression and activity is inhibited by thyroglobulin (Tg), tumour necrosis factor alpha (TNF-α), transforming growth factor beta 1 (TGF-β1), interleukin 6 (IL-6) and Interleukin 1 beta (IL-1β), interferon-γ (IFN-γ), insulin like growth factor 1 (IGF-1) and phosphoinositide 3-kinase (PI3K) and how fluoride upregulates expression and activity of these biomarkers. I further describe the crucial role of prolactin and megalin in regulation of NIS expression and iodine homeostasis and the effect of fluoride in down regulating prolactin and megalin expression. Among many other issues, I discuss the potential conflict between public health policies such as water fluoridation and its contribution to iodine deficiency, neurodevelopmental and pathological disorders. Further studies are warranted to examine these associations.