EFSA NDA Panel (EFSA Panel on Dietetic Products, Nutrition and Allergies), 2013 . Scientific opinion on Dietary Reference Values for fluoride

Following a request from the European Commission, the Panel on Dietetic Products, Nutrition and Allergies (NDA) derived Dietary Reference Values (DRVs) for fluoride, which are provided as Adequate Intake (AI) from all sources, including non-dietary sources. Fluoride is not an essential nutrient. Therefore, no Average Requirement for the performance of essential physiological functions can be defined. Nevertheless, the Panel considered that the setting of an AI is appropriate because of the beneficial effects of dietary fluoride on prevention of dental caries. The AI is based on epidemiological studies (performed before the 1970s) showing an inverse relationship between the fluoride concentration of water and caries prevalence. As the basis for defining the AI, estimates of mean fluoride intakes of children via diet and drinking water with fluoride concentrations at which the caries preventive effect approached its maximum whilst the risk of dental fluorosis approached its minimum were chosen. Except for one confirmatory longitudinal study in US children, more recent studies were not taken into account as they did not provide information on total dietary fluoride intake, were potentially confounded by the use of fluoride-containing dental hygiene products, and did not permit a conclusion to be drawn on a dose-response relationship between fluoride intake and caries risk. The AI of fluoride from all sources (including non-dietary sources) is 0.05 mg/kg body weight per day for both children and adults, including pregnant and lactating women. For pregnant and lactating women, the AI is based on the body weight before pregnancy and lactation. Reliable and representative data on the total fluoride intake of the European population are not available

Chelation in Metal Intoxication

Chelation therapy is the preferred medical treatment for reducing the toxic effects of metals. Chelating agents are capable of binding to toxic metal ions to form complex structures which are easily excreted from the body removing them from intracellular or extracellular spaces. 2,3-Dimercaprol has long been the mainstay of chelation therapy for lead or arsenic poisoning, however its serious side effects have led researchers to develop less toxic analogues. Hydrophilic chelators like meso-2,3-dimercaptosuccinic acid effectively promote renal metal excretion, but their ability to access intracellular metals is weak. Newer strategies to address these drawbacks like combination therapy (use of structurally different chelating agents) or co-administration of antioxidants have been reported recently. In this review we provide an update of the existing chelating agents and the various strategies available for the treatment of heavy metals and metalloid intoxications

The Effect of Altering Trace Element Status on The Progress of Lead Toxicity in The Rat

125 p.Thesis (Ph.D.)--University of Illinois at Urbana-Champaign, 1976.U of I OnlyRestricted to the U of I community idenfinitely during batch ingest of legacy ETD

The Alchemist’s Approach to Metal Poisoning: Transforming the Metal Burden

Metal poisoning is a global problem with humans being exposed to a wide range of metals in varying doses and varying time frames. Traditionally, treatment involves removal of the toxic source or chelation therapy. An intermediate approach is needed. This review outlines the argument for the use of essential metal supplementation as a strategy to induce metallothionein expression and displace the toxic metal from important biological systems, improving the metal burden of the patient. Specific recommendations are given for supplementation with calcium, zinc and vitamin E as a broad strategy to improve the status of those exposed to toxic metals

Studies of zinc metabolism in pregnant and lactating rats

The metabolism of 65Zn administered intramuscularly (Expt 1) or enterally (Expt 2) at the beginning of pregnancy in rats given a control or marginal-Zn diet was measured. In Expt 2 a comparison was also made between pregnant and non-pregnant rats. The loss of 65Zn (assumed to represent labile body Zn) was markedly reduced in animals fed on a marginal-Zn diet compared with controls, and this effect occurred very rapidly, i.e. within 48 h of introducing the marginal-Zn diet. Pregnancy itself had a much less important effect on 65Zn turnover than diet. Transfer of 65Zn to the litter was significantly greater in the animals fed on a marginal-Zn diet compared with controls but total Zn transfer was reduced. The effect of length of time on a marginal-Zn diet on fetal growth and composition was examined. Compared with controls, fetal weight was significantly greater in litters from mothers fed on a marginal-Zn diet during the last 4, 7 or 14 d of pregnancy, but no different in litters from mothers fed on a marginal-Zn diet throughout pregnancy. There were no differences in the proportions of protein or fat in the fetuses from mothers fed on the control or marginal-Zn diets but the Zn concentration was lower in litters from mothers fed on a marginal-Zn diet during part or all of the pregnancy when compared with controls. The transfer of 65Zn from mothers to litters during birth and the first 3 d of lactation was measured. There were no differences in maternal or litter 65Zn just before or just after birth, but within 72 h maternal 65Zn had significantly decreased and litter 65Zn increased. Increases in litter size were associated with greater total litter 65Zn but reduced individual fetal 65Zn. These experiments demonstrate the importance of an adequate daily supply of Zn during pregnancy. Although there is room for adaptation to a marginal-Zn intake (by reducing Zn excretion) the maintenance of Zn homeostasis is only possible in the absence of other forms of stress, such as pregnancy, to the body. The consequence of insufficient Zn at times of rapid fetal growth on carbohydrate and lipid metabolism warrants further investigation