Fluoride’s toxicity is significantly enhanced in the presence of nutritional deficiencies. Similarly, fluoride exposure increases the body’s requirement for certain nutrients. An individual with a high intake of fluoride, for example, will need a proportional increase in calcium to avoid the mineralization defects (e.g., osteomalacia) that fluoride causes to bone tissue. Fluoride also appears to increase the metabolic requirement for magnesium, by sequestering it into the skeleton and thereby making magnesium less available to other tissues. As described by the National Research Council of Canada (NRCC):
“Pita et al. (1972) have shown that fluoride supplements increased the magnesium content of mineralized tissues in rats. Ophaug and Singer (1976) reported that fluoride exerted a significant effect in retarding the mobilization of skeletal magnesium in rats. O’Dell et al. (1973) observed that fluoride had a ‘magnesium-sparing’ effect in Guinea pigs, but found that high fluoride supplements were toxic when magnesium was severely limited. O’Dell et al. concluded that ‘a high intake of magnesium should be highly beneficial in areas where fluorosis prevails.’ Thus, there is evidence that fluoride intake can increase the long-term metabolic requirement for magnesium.” (Marier & Rose 1977).
Consistent with the NRCC’s concern, a recent study of dialysis patients from Toronto found that bone fluoride content was significantly correlated with bone magnesium content, (Ng 2004), while a recent study of skeletal fluorosis patients in Turkey found “that chronic fluorosis is associated with reduced serum levels of magnesium.” (Ersol 2011).
Importantly, some research has found that patients with Repetitive Stress Injury (RSI) can experience significant recovery in their symptoms by reducing their fluoride intake while increasing their magnesium intake. According to Smith (1985):
In 12 RSI subjects fluoride (F-) levels in bone were appreciably higher than 12 appropriate controls. Estimates of dietary intake of RSI subjects, revealed a Mg2+ deficit and an excessive F_ intake. Fluorotic bone has an increased Mg2+ content possibly due to some deposition of MgF2. The amorphous phase in bone may act as a “reservoir” of ions available to regulate plasma Ca, PO4 and Mg2+ levels. Fluoride accumulates in bone with age, especially in areas of active ossification. A locally raised F concentration in an osteocyte lacunae (during resorption) could interfere with normal functioning of the cell, or trigger the precipitation of crystalline apatite, or lead to the formation of MgF2. Any one of these reactions might interfere with the passage of Mg 2+ ions from the bone “reservoir” into circulating extracellular fluid. A localized Mg2+ deficiency could disturb pyrophosphate metabolism and lead to deposition of Ca salts in sensitive areas. Through adjustment of dietary intake of the previously mentioned 12 RSI subjects which included more Mg2+ and less F-, eight of the subjects experienced marked relief from previously painful RSI symptoms after a six week test period.
Ersoy IH, et al. (2011). Serum copper, zinc, and magnesium levels in patients with chronic fluorosis. Biol Trace Elem Res. 143(2):619-24.
Marier J, Rose D. 1977. Environmental Fluoride. National Research Council of Canada. Associate Committe on Scientific Criteria for Environmental Quality. NRCC No. 16081.
Ng AHM, et al. (2004). Association between fluoride, magnesium, aluminum and bone quality in renal osteodystrophy. Bone 34: 216-224.
Smith GE. (1985). Repetititive Strain Injury (RSI) and Magnesium and Fluoride Intake. New Zealand Medical Journal 98:556-57. [See study]