Fluoridated Water Can Calcify Arteries, Study Finds

“There was significant correlation between history of cardiovascular events and presence of fluoride uptake in coronary arteries. The coronary fluoride uptake value in patients with cardiovascular events was significantly higher than in patients without cardiovascular events.”

The argument, at the time, was the study was simply about a new diagnostic technique and shouldn’t be ‘read into,’ and that, presumably, the increased fluoride uptake value observed in patients with a higher frequency of cardiovascular events was a an ‘effect’ of the heart disease itself and not in any way indicative of fluoride’s causative role as a cardiotoxic agent — despite the fact that fluoride’s cardiotoxicity has already been consistently demonstrated in the biomedical literature.

Now, a provocative new study published in the journal Toxicology not only provides some vindication for our previous interpretations, but also raises serious concern over the cardiovascular complications associated with water fluoridation practices, showing for the first time that despite exhibiting an anti-calcification effect in vitro (cell model) fluoride exposure at levels found in people who drink fluoridated water exhibits artery-calcifying effects in the more important in vivo (animal) model.

Titled, “Effect of water fluoridation on the development of medial vascular calcification in uremic rats” the study opens with a description of the common medical justification for public water fluoridation:

“In order to improve dental health in the population, fluoride is included in tooth pastes and mouthwash solutions or is added to public water supplies at 0.5–1.5 mg/L (WHO, 2008), which has been a common practice in some countries since 1945.”

And yet, the study acknowledges that fluoride is a well-established toxicant that our body has to either incorporate into its tissues or excrete through the kidney’s to sequester or eliminate:

“More than 90% of ingested fluoride is absorbed through the intestine and quickly distributed between plasma/soft tissues and calcified structures, where it can be sequestered for years (Buzalaf and Whitford, 2011). When water is fluoridated at the WHO- recommended levels, the range of plasma fluoride concentration is usually 1–6 uM (Husdan et al., 1976; Singer and Ophaug, 1979). Fluoride is not under homeostatic control, and it is cleared from the plasma within few hours by the complementary action of calcified tissues and the kidneys.”

Those with chronic kidney disease have a harder time clearing the fluoride, which results in increased blood plasma levels, especially as the length of exposure increases.

The study noted that in healthy people, almost without exception, fluoride accumulates in the aorta, and in the elderly can exceed 100 ug/g [microgram/gram] tissue. Since atherosclerosis involves the gradual hardening and final calcification of the arteries with a form of calcium known as hydroxylapatite, fluoride’s role in replacing hydroxyls within hydroxylapatite crystals to form fluorapatite can be considered enhancing the cardiotoxicity of these calcium deposits due to the fact that fluorapatite is less soluble than hydroxylapatite and therefore more resistant to the body’s demineralization mechanisms (or de-calcification with natural substances such as magnesium, hawthorn or vitamin K2). The authors address this point:

“From a therapeutic point of view, this incorporation [of fluoride into hydroxylapatite as fluorapatite] may involve an additional problem, because these calcifications will be more difficult to eliminate, if at all possible.”

The report discussed how despite the observation that fluoride accumulates in the main arteries, “the effects on the vascular wall are not clear.” A brief review of the literature shows highly contradictory results, with some studies implying fluoride exposure actually reduces aortic calcification and others showing (as would be expected) deleterious effects on the cardiovascular system. This uncertainty was one of the main reasons they designed their study:

“The aforementioned divergent findings can be explained by the use of different procedures, including very high doses of fluoride, the duration of treatment, and the animal species, in addition to either an experimental or epidemiological setup. In this work, our objective was to clarify the effect of fluoride, if any, on the development and course of medial vascular calcification (MVC, Mönckeberg’s sclerosis) in uremic rats, using low, recommended concentrations in drinking water. Our rationale was that de novo calcified tissue in aorta should incorporate fluoride when exposure to this halogen is concomitant with the course of calcification, and subsequently the rate of calcium phosphate crystallization and/or mineralization should be altered, similar to the effects in tooth enamel or bone. We used two established experimental models of calcification, rat aortic smooth muscle cells incubated with 2 mM Pi, and rats with 5/6-nephrectomy [5/6th of their kidneys removed to model chronic kidney disease] and fed a Pi-enriched diet [Pi = Inorganic phosphate], in combination with low concentrations of fluoride (similar to that of public water fluoridation). Our findings have shown that the results are inverse depending on the experimental model, which highlights the need to carry out in vivo approaches when studying complex multifactorial processes, such as Mönckeberg’s sclerosis [a type of arterial calcification].”

The study found a striking contrast between the in vitro (cell model) and in vivo (animal model) results: within the former, fluoride prevented calcification, within the later, it enhanced medial [middle portion of the artery] vascular calcification in the arteries of animals whose kidneys were weakened. Keep in mind that they did not use ‘mega doses’ of fluoride in the animal study, opting for the administration of the World Health Organization’s recommended concentration of fluoride in public drinking water to ‘prevent cavities.’

The researchers determined that fluoride’s adverse effects on vascular function in the animal model were mediated by the inherent kidney-damaging properties of fluoride (nephrotoxicity). Whereas healthy individuals are not prone to significant or at least acutely discernible damage from low level fluoride exposure (though some functional damage and proteomic changes are observed at 5-8 ppm), those with chronic kidney disease (CKD), have impaired fluoride clearance, subsequent elevated plasma fluoride levels, which creates a vicious self-perpetuating cycle of fluoride-induced aggravation of their decline in kidney function.

The researchers summarized their main finding as follows:

“The main conclusion of our study is that CKD is aggravated even by low concentrations of fluoride, which in turn accelerates medial vascular calcification (MVC), thereby confirming and extending previous reports on fluorosis in CKD patients exposed to WHO-recommended fluoride concentrations in drinking water (Greenberg et al., 1974; Lyaruu et al., 2008).”

Their final comments are to call for a reappraisal of the risks/benefits associated with fluoridation of municipal drinking water:

“In summary, the effects of fluoride on renal function and vascular health are more complicated than expected. Our findings could help to decide whether the use of fluoride to improve the dental health of the population through indiscriminate practices, such as adding it to municipal drinking water, should be reconsidered and should be replaced by a fluoridation policy based on the health status of individuals.”

It should be noted that fluoride’s association with soft tissue calcification also extends to brain structures, including the pineal gland, which we documented in a previous article: Fluoride: Calcifier of the Soul, and that its neurotoxicity — especially as evidenced by lowered I.Q. — is well documented.