The kidneys help prevent the build-up of toxic fluoride levels in the body by excreting fluoride through the urine. When kidney function declines (due to age or disease), the risk of fluoride toxicity increases.
Individuals with advanced kidney disease are known to have a very high susceptibility to fluoride toxicity since their bones and other tissues accumulate fluoride at levels far higher than healthy individuals. This fluoride build-up places kidney patients at a sharply elevated risk for skeletal fluorosis, a painful bone disease caused by excessive fluoride intake. Fluoride intake can also contribute to and exacerbate the complex bone disease renal osteodsystrophy, as well as the tooth staining and disfigurations that many people with advanced kidney disease suffer. These risks exist at current levels of exposure in communities with fluoridated drinking water.
Fluoride & Osteomalacia
Excessive intake of fluoride is well known to cause osteomalacia, a bone-softening disease which frequently develops in advanced kidney disease. The link between fluoride and osteomalacia started receiving attention in the 1970s when researchers discovered that the failure by dialysis centers to filter fluoride out of the water used in dialysis was causing severe, debilitating osteomalacia in the patients. By the start of the 1980s, therefore, all dialysis units had installed filtration equipment to remove the fluoride.
Current Fluoride Exposures Linked to Osteomalacia in Dialysis Patients
Recent research shows that dialysis patients still face elevated risks of fluoride-induced osteomalacia, not because of the dialysis itself, but because of everyday fluoride exposures from water and other dietary sources.
In 2004, researchers from Toronto, Canada reported that dialysis patients with osteomalacia have notably high levels of fluoride in their bone (avg. 3,400 ppm), even when compared to other dialysis patients (2,400-2,700 ppm). Further, the researchers reported that the level of fluoride in the patients’ bone was significantly correlated to the quantity of osteoid, a type of unmineralized tissue. An excessive quantity of osteoid in bone is the hallmark of osteomalacia. According to the researchers: “Fluoride interfered with bone mineralization and increased osteoid content, which was most evident in osteomalacia and the mixed bone disorder.” (Ng 2004).
Low Levels of Fluoride Linked to Skeletal Fluorosis
In 1979, scientists at the Mayo Clinic documented the occurrence of crippling skeletal fluorosis in patients with advanced kidney disease drinking water with just 1.7 ppm fluoride. (Johnson 1979). Based on these findings, the authors reasoned that a similar risk would likely exist at the fluoride level (1 ppm) added to water to prevent tooth decay. Despite the Mayo Clinic’s findings, and despite numerous calls for studies to determine the rate of skeletal fluorosis among people with kidney disease, there has yet to be a single such study in the United States or any other fluoridating country, to determine the prevalence of skeletal fluorosis, or more subtle indications of fluoride toxicity, among patients with kidney disease. Read more.
Some Cases of Renal Osteodystrophy Are Likely Skeletal Fluorosis
Several lines of evidence suggest that some cases of “renal osteodystrophy” may actually be skeletal fluorosis, or a combination of both. This possibility is supported by the Mayo Clinic’s findings of skeletal fluorosis at low levels of fluoride intake and by the fact that the bone changes in renal osteodystrophy can closely resemble the bone changes in skeletal fluorosis. Further, it has become clear that many doctors in the United States have failed to diagnose skeletal fluorosis, even when it is present in its most crippling form. Dr. Helmut Schiffl, a scientist who has published several studies on the handling of fluoride in kidney disease, has explained some of the reasons why skeletal fluorosis in kidney disease likely goes undiagnosed:
“The safety margin for exposure to fluoride by renal patients is unknown, measurements of fluoride levels are not routine, the onset of skeletal fluorosis is slow and insidious, clinical symptoms of this skeletal disorder are vague, progression of renal functional decline is multifactorial and physicians are unaware of side effects of fluoride on kidneys or bone.”
Children with Kidney Disease Are at Risk for Severe Dental Fluorosis
As with adults, children with kidney disease have a heightened susceptibility to fluoride toxicity. In addition to bone damage, children with kidney disease are at high risk of developing disfiguring forms of dental fluorosis, a discoloration and pitting of teeth caused by excess fluoride intake during early childhood. Fluoride also likely plays a role in the high rate of enamel defects (“enamel hypoplasia”) that children with kidney disease are known to have. Such defects, which can be very similar in appearance to fluorosis, may sometimes be fluorosis that is misdiagnosed. Read more.
Fluoride Can Damage the Kidney Itself
Because the kidney is exposed to higher concentrations of fluoride than all other soft tissues (with the possible exception of the bladder and pineal gland), there is concern that excess fluoride exposure may contribute to kidney disease, initiating a “vicious cycle” where the damaged kidneys increase the accumulation of fluoride, causing in turn further damage to the kidney, bone, and other organs.
This possibility is supported by both animal and human studies. In animals, kidney damage has been reported at levels as low as 1 ppm if the animals consume the water for long periods of time. In humans, elevated rates of kidney damage are frequently encountered among populations with skeletal fluorosis. In addition, several case reports suggest that some individuals with kidney disease can experience significant recovery in their clinical signs and symptoms following the provision of fluoride-free water.
New Facts on Fluoridation
[NOTE: The first quarter of this article from SATURDAY REVIEW - which is not reproduced below - covers the findings of a 1965 paper from the journal Archives of Internal Medicine, authored by Dr. Donald Taves of the University of Rochester. In the paper, Taves documented high levels of fluoride
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