Abstract
This study was conducted to determine whether feeding a diet containing excess crude protein (CP) or calcium (Ca) for up to 120 days can ameliorate the effects of fluoride (F) intake on bone health and thyroid function observed in rabbits fed a CP- and Ca-deficient diet. Treatment with F increased serum bone Gla protein concentrations and effects of F were reversed within 60 days in animals fed a high Ca diet. Feeding either a high CP or high Ca diet for 60–90 days increased combined cortical thickness (CCT) and the ratio of CCT to medullary canal diameter (MCD) in the midshaft of the femur of F treated animals. Bone mineral content was also reduced in response to F treatment and effects of F were reversed in animals fed a high CP diet for 30 days. Feeding a high Ca diet reversed F-induced alterations in serum TSH concentrations on day 30 and day 120 and on serum T3 levels by day 90. In contrast, F-induced elevations in serum T4 at day 30 and day 60 were reversed in animals fed a high CP or high Ca diet. Although no effect of F treatment on serum free T3 levels was noted, free T4 was elevated on day 30 in response to F treatment and the F-induced elevation in free T4 was not observed in animals fed a high CP diet. These results demonstrate divergent protective effects of high CP and high Ca diets on adverse indices of bone metabolism and thyroid function induced by F treatment in rabbits fed a CP- or Ca-deficient diet.
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Fluoride-induced thyroid dysfunction in rats: roles of dietary protein and calcium level.
To assess the roles of dietary protein (Pr) and calcium (Ca) level associated with excessive fluoride (F) intake and the impact of dietary Pr, Ca, and F on thyroid function, 144 30-day-old Wistar albino rats were randomly allotted to six groups of 24 (female:male = 1:1). The six groups were
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Prevalence and aetiology of juvenile skeletal fluorosis in the south-west of the Hai district, Tanzania--a community-based prevalence and case-control study
INTRODUCTION: Fluorosis is endemic throughout the East African Rift valley, including parts of Tanzania. The aim of the study was to identify all cases of deforming juvenile skeletal fluorosis (JSF) in a northern Tanzanian village and to document the extent of dental fluorosis (DF). METHODS: Door-to-door prevalence survey of all residents
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The effect of nutrition on the development of endemic osteomalacia in patients with skeletal fluorosis
The aim of the study was to study the relationship between nutrition and endemic osteomalacia, resulting in bone deformation with hump back, spinal curvature and "0" legs, in persons living in high drinking water fluoride areas with skeletal fluorosis. A dietary survey was made of 30-50 families from each of
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[Effects of excess fluoride on bone turnover under conditions of diet with different calcium contents].
OBJECTIVE: To study the effects of excess fluoride on bone turnover under conditions of diet containing different amount of calcium. METHODS: The experiment was performed on rats raised on a balanced diet with adequate calcium or a monotonous diet with low calcium and given amount of fluoride in their drinking water
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Analysis of the roles of dietary protein and calcium in fluoride-induced changes in T-lymphocyte subsets in rat
The roles of dietary protein (Pr) and calcium (Ca) levels on the changes in T-lymphocyte subsets induced by excessive fluoride (F) intake were assessed using rats that were malnourished for 120 days as a model. The CD4+ and CD8+ T-lymphocytes in the spleen tissue were determined by flow cytometry and
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Nutrient Deficiencies Enhance Fluoride Toxicity
It has been known since the 1930s that poor nutrition enhances the toxicity of fluoride. As discussed below, nutrient deficiencies have been specifically linked to increased susceptibility to fluoride-induced tooth damage (dental fluorosis), bone damage (osteomalacia), neurotoxicity (reduced intelligence), and mutagenicity. The nutrients of primary importance appear to be calcium,
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Fluoride's Impact on Thyroid Hormones
Up through the 1950s, doctors in Europe and South America prescribed fluoride for this purpose in patients with hyperthyroidism. (Merck Index 1968). Fluoride was selected as a thyroid suppressant based on findings dating back to the mid-19th century that fluoride is a goitrogen (a substance that can cause goiter). When used as
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Fluoride Exposure Aggravates the Impact of Iodine Deficiency
A consistent body of animal and human research shows that fluoride exposure worsens the impact of an iodine deficiency. Iodine is the basic building block of the T3 and T4 hormones and thus an adequate iodine intake is essential for the proper functioning of the thyroid gland. When iodine intake is inadequate during infancy and
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Mayo Clinic: Fluoridation & Bone Disease in Renal Patients
The available evidence suggests that some patients wtih long-term renal failure are being affected by drinking water with as little as 2 ppm fluoride. The finding of adverse effects in patients drinking water with 2 ppm of fluoride suggests that a few similar cases may be found in patients imbibing 1 ppm, especially if large volumes are consumed, or in heavy tea drinkers. The finding of adverse effects in patients drinking water with 2 ppm of fluoride suggests that a few similar cases may be found in patients imbibing 1 ppm, especially if large volumes are consumed, or in heavy tea drinkers and if fluoride is indeed the cause. It would seem prudent, therefore, to monitor the fluoride intake of patients with renal failure living in high fluoride areas.
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"Pre-Skeletal" Fluorosis
As demonstrated by the studies below, skeletal fluorosis may produce adverse symptoms, including arthritic pains, clinical osteoarthritis, gastrointestinal disturbances, and bone fragility, before the classic bone change of fluorosis (i.e., osteosclerosis in the spine and pelvis) is detectable by x-ray. Relying on x-rays, therefore, to diagnosis skeletal fluorosis will invariably fail to protect those individuals who are suffering from the pre-skeletal phase of the disease. Moreover, some individuals with clinical skeletal fluorosis will not develop an increase in bone density, let alone osteosclerosis, of the spine. Thus, relying on unusual increases in spinal bone density will under-detect the rate of skeletal fluoride poisoning in a population.
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