the parathyroid or the thyroid parafollicular cells leads to a compensatory response from the other, but this has not been examined.

Several studies have reported different responses among individuals or variability in group responses (Teotia and Teotia 1973; Teotia et al. 1978; Krishnamachari 1986; Duursma et al. 1987; Dandona et al. 1988; Stamp et al. 1988; 1990; Jackson et al. 1994; Dure-Smith et al. 1996; Gupta et al. 2001); the reasons for these differences are not clear but might include genetic differences in addition to variability in nutritional factors. The effects also might vary with age, sex, and the duration (as well as degree) of hypocalcemia.

Any cause of hypocalcemia or vitamin D deficiency can lead to secondary hyperparathyroidism (elevated PTH) in an attempt by the body to maintain calcium homeostasis (Ahmad and Hammond 2004).9 Fluoride clearly has the effect of decreasing serum calcium and increasing the calcium requirement in some or many exposed persons. In those studies which have measured it, PTH is elevated in some persons in response to fluoride exposure, indicating secondary hyperparathyroidism. No information has been reported in those studies on the clinical effects, if any, in those persons. In general, secondary hyperparathyroidism in response to calcium deficiency may contribute to a number of diseases, including osteoporosis, hypertension, arteriosclerosis, degenerative neurological diseases, diabetes mellitus, some forms of muscular dystrophy, and colorectal carcinoma (Fujita and Palmieri 2000). McCarty and Thomas (2003) suggest that down-regulation of PTH (by calcium and/or vitamin D supplementation) could assist in control of weight and prevention of diabetes.

Calcium deficiency induced or exacerbated by fluoride exposure may contribute to other adverse health effects. For example, Goyer (1995) indicates that low dietary calcium increases the concentration of lead in critical organs and the consequent toxicity. A recent increase in the number of cases of nutritional rickets in the United States appears to reflect calcium-deficient diets rather than vitamin D deficiencies (DeLucia et al. 2003). These cases occur in children whose diet lacks dairy products;10 circulating PTH concentrations are elevated, as are alkaline phosphatase concentrations. The authors “emphasize that nutritional calcium deficiency may occur in North American infants and is not limited to the setting of developing countries” and state that “factors that affect calcium absorption may be important in determining a susceptibility to the development of rickets.”


Renal failure is the most common cause of secondary hyperparathyroidism (Ahmad and Hammond 2004).


A diet low in dairy products will have not only a lower calcium content but probably also a higher fluoride content, due to greater use of beverages such as juices that have been manufactured with fluoridated municipal water (see Chapter 2); absorption and retention of fluoride will be higher because of the calcium deficiency.

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