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Twenty calves were placed on study at 3 days of age and were placed according to birth order into one of two groups: SS, which received 0.05% BW sodium zeolite A (SZA) added to their milk replacer, and CO, which received only milk replacer. Blood samples were taken on days 0, 30, and 60 for osteocalcin (OC) and deoxypyridinoline (DPD) analysis. On day 60, the calves were euthanized, and synovial fluid, articular cartilage, and both fused metacarpals were collected for bone quality analyses such as architecture and mechanical properties, mineral composition, and glycosaminoglycan concentration. There were no differences in OC concentrations because of treatment (p = 0.12), and CO calves had lower DPD concentrations than SS calves (p = 0.01), but the OC-to-DPD ratio was not different between treatments (p = 0.98). No differences in bone architecture or mechanical properties were detected. SZA supplementation increased cortical bone (p = 0.0002) and articular cartilage (p = 0.05) aluminum content. Glycosaminoglycan concentrations were not different in synovial fluid or cartilage. Supplementation of SZA appeared to alter the rate of bone turnover without altering bone strength. Aluminum concentrations in the bone and cartilage increased, which may be a concern, although the long-term consequences of such remain to be determined.

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The objective was to determine the effects of sodium zeolite A (SZA) on mineral metabolism and tissue mineral composition in calves. Twenty calves were placed on study at 3 days of age and were placed into one of two groups: SS, which received 0.05% BW SZA added to their milk replacer, and CO, which received only milk replacer. Blood samples were taken on days 0, 30, and 60 for mineral analysis. Urine and feces were collected on day 30 for mineral metabolism, and on day 60, the calves were euthanized, and samples were taken from numerous organs for mineral analyses. Aluminum retention was increased in the SS calves (p = 0.001). Silicon concentrations were increased in the aorta, spleen, lung, muscle, and kidney of the SS calves, and aluminum was increased in all SS tissues (p < 0.05). Calcium concentrations were increased in aorta, liver, muscle, and tendon; phosphorus concentrations were increased in aorta, but decreased in plasma; magnesium concentrations were increased in aorta, heart, kidney, liver, and pancreas, but decreased in plasma; and iron concentrations were decreased in kidney and liver (p < 0.05). The accumulation of tissue aluminum and therefore potential adverse consequences may preclude any benefits of using SZA as a dietary supplement.

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Magnesium is involved in numerous processes that affect muscle function including oxygen uptake, energy production and electrolyte balance. Thus, the relationship between magnesium status and exercise has received significant research attention. This research has shown that exercise induces a redistribution of magnesium in the body to accommodate metabolic needs. There is evidence that marginal magnesium deficiency impairs exercise performance and amplifies the negative consequences of strenuous exercise (e.g., oxidative stress). Strenuous exercise apparently increases urinary and sweat losses that may increase magnesium requirements by 10-20%. Based on dietary surveys and recent human experiments, a magnesium intake less than 260 mg/day for male and 220 mg/day for female athletes may result in a magnesium-deficient status. Recent surveys also indicate that a significant number of individuals routinely have magnesium intakes that may result in a deficient status. Athletes participating in sports requiring weight control (e.g., wrestling, gymnastics) are apparently especially vulnerable to an inadequate magnesium status. Magnesium supplementation or increased dietary intake of magnesium will have beneficial effects on exercise performance in magnesium-deficient individuals. Magnesium supplementation of physically active individuals with adequate magnesium status has not been shown to enhance physical performance. An activity-linked RNI or RDA based on long-term balance data from well-controlled human experiments should be determined so that physically active individuals can ascertain whether they have a magnesium intake that may affect their performance or enhance their risk to adverse health consequences (e.g., immunosuppression, oxidative damage, arrhythmias).

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OBJECTIVES: To determine whether moderately high or low intakes of zinc adversely affect the copper status of postmenopausal women to result in unfavorable changes in calcium and magnesium metabolism and other indicators of bone turnover. DESIGN: After a 10-day equilibration period in which the diet provided 31.5 micromol (2 mg) Cu and 137.7 micromol (9 mg) Zn/8.4 MJ (2000 kcal), the subjects were randomly divided into two groups, with one group fed the basal diet supplemented to provide 15.7 micromol (1 mg) Cu/8.4 MJ, and the other group fed the same diet supplemented to provide 47.2 micromol (3 mg) Cu/8.4 MJ. After equilibration, both groups were fed the basal diet with no zinc supplemented (provided 45.9 micromol [3 mg] Zn/8.4 MJ) for 90 days; this was followed by another 10-day equilibration period before the basal diet was supplemented with zinc to provide 811 micromol (53 mg)/8.4 MJ for 90 days. SETTING: The metabolic unit of the Grand Forks Human Nutrition Research Center, Grand Forks, ND, USA. SUBJECTS: A total of 28 postmenopausal women recruited by advertisement throughout the United States of America. Among them, 25 women (64.9+6.7 y) completed the study; 21 as designed. RESULTS: The moderately high intake compared to the low intake of zinc increased the excretion of magnesium in the feces and urine, which resulted in a decreased magnesium balance. In the women fed low dietary copper, plasma osteocalcin was higher during the low-zinc than high-zinc dietary period. The urinary excretion of N-telopeptides was increased and the serum calcitonin concentration was decreased by high dietary zinc regardless of dietary copper. CONCLUSIONS: A moderately high intake of zinc (811 micromol/day; 53 mg/day) did not induce changes in copper metabolism that resulted in unfavorable changes in bone or mineral metabolism. However, low dietary zinc (45.9 micromol/day; 3 mg/day) apparently resulted in undesirable changes in circulating calcitonin and osteocalcin. As a moderately high intake of zinc decreased magnesium balance, further study of the possibility that a high intake of zinc is a health concern for individuals consuming less than the recommended amounts of magnesium is warranted.

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Both arginine and silicon affect collagen formation and bone mineralization. Thus, an experiment was designed to determine if dietary arginine would alter the effect of dietary silicon on bone mineralization and vice versa. Male weanling Sprague-Dawley rats were assigned to groups of 12 in a 2 x 2 factorially arranged experiment. Supplemented to a ground corn/casein basal diet containing 2.3 microg Si/g and adequate arginine were silicon as sodium metasilicate at 0 or 35 microg/g diet and arginine at 0 or 5 mg/g diet. The rats were fed ad libitum deionized water and their respective diets for 8 wk. Body weight, liver weight/body weight ratio, and plasma silicon were decreased, and plasma alkaline phosphatase activity was increased by silicon deprivation. Silicon deprivation also decreased femoral calcium, copper, potassium, and zinc concentrations, but increased the femoral manganese concentration. Arginine supplementation decreased femoral molybdenum concentration but increased the femoral manganese concentration. Vertebral concentrations of phosphorus, sodium, potassium, copper, manganese, and zinc were decreased by silicon deprivation. Arginine supplementation increased vertebral concentrations of sodium, potassium, manganese, zinc, and iron. The arginine effects were more marked in the silicon-deprived animals, especially in the vertebra. Germanium concentrations of the femur and vertebra were affected by an interaction between silicon and arginine; the concentrations were decreased by silicon deprivation in those animals not fed supplemental arginine. The change in germanium is consistent with a previous finding by us suggesting that this element may be physiologically important, especially as related to bone DNA concentrations. The femoral and vertebral mineral findings support the contention that silicon has a physiological role in bone formation and that arginine intake can affect that role.

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We have shown that silicon (Si) deprivation decreases the collagen concentration in bone of 9-wk-old rats. Finding that Si deprivation also affects collagen at different stages in bone development, collagen-forming enzymes, or collagen deposition in other tissues would have implications that Si is important for both wound healing and bone formation. Therefore, 42 rats in experiment 1 and 24 rats in experiment 2 were fed a basal diet containing 2 or 2.6 microg Si/g, respectively, based on ground corn and casein, and supplemented with either 0 or 10 microg Si/g as sodium metasilicate. At 3 wk, the femur was removed from 18 of the 42 rats in experiment 1 for hydroxyproline analysis. A polyvinyl sponge was implanted beneath the skin of the upper back of each of the 24 remaining rats. Sixteen hours before termination and 2 wk after the sponge had been implanted, each rat was given an oral dose of 14C-proline (1.8 microCi/100 g body wt). The total amount of hydroxyproline was significantly lower in the tibia and sponges taken from Si-deficient animals than Si-supplemented rats. The disintegrations per minute of 14C-proline were significantly higher in sponge extracts from Si- deficient rats than Si-supplemented rats. Additional evidence of aberrations in proline metabolism with Si deprivation was that liver ornithine aminotransferase was significantly decreased in Si-deprived animals in experiment 2. Findings of an increased accumulation of 14C-proline and decreased total hydroxyproline in implanted sponges and decreased activity of a key enzyme in proline synthesis (liver ornithine aminotransferase) in Si-deprived animals indicates an aberration in the formation of collagen from proline in sites other than bone that is corrected by Si. This suggests that Si is a nutrient of concern in wound healing as well as bone formation.

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Sporadic reports have appeared that suggest silicon plays a functional role in immune function by affecting lymphocyte proliferation. In addition, there is also considerable interest in supplemental arginine as a modulator of immune function. Therefore, the purpose of this animal experiment was to determine the effect of supplemental compared to adequate arginine on immune function as measured by splenic T-lymphocyte proliferation in the presence of adequate or inadequate dietary silicon. The independent variables were, per gram of fresh diet, silicon supplements of 0 or 35 microg and arginine supplements of 0 or 5 mg. The basal diet contained 2.3 microg silicon/g and 7.82 mg L-arginine/g. After feeding the male rats (nine per treatment group) for 8 wk, spleen lymphoid cells were isolated and cultured with methyl-3[H]thymidine. Supplemental arginine significantly decreased Con-A-induced DNA synthesis of splenic T-lymphocytes, but the response to arginine was influenced by dietary silicon. The decreased DNA synthesis was more marked when rats were fed adequate silicon than when fed inadequate silicon. Also, when arginine was not supplemented, DNA synthesis was higher in lymphocytes from rats fed an adequate silicon diet than rats fed the inadequate silicon diet. These findings support the huypothesis that an interaction between silicon and arginine affects immune function and that inadequate dietary silicon impairs splenic lymphocyte proliferation in response to an immune challenge.

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OBJECTIVES: To better define the relationship between dietary zinc and copper for humans so that sound recommendations for intakes of these elements can be made. METHODS: A study was conducted to ascertain the effect of moderately excessive and deficient intakes of zinc on copper metabolism and use in humans fed low and luxuriant amounts of copper. Twenty-one postmenopausal women housed in a metabolic unit completed the study as designed. After a 10-d equilibration period in which they were fed a diet providing 31.5 micromol (2 mg) Cu and 91.8 micromol (9 mg) Zn/8.4 MJ (2000 kcal), the women were divided into two groups. One group was fed a diet containing 15.7 micromol (1 mg) Cu/8.4 MJ (2000 kcal), and the other group was fed a diet containing 47.2 micromol (3 mg) Cu/8.4 MJ (2000 kcal). After equilibration, both groups were fed the basal diet providing 45.9 micromol (3 mg) Zn/8.4 MJ (2000 kcal) for 90 d; this was followed by another 10-d equilibration period before dietary zinc was increased to 811 micromol (53 mg)/8.4 MJ (2000 kcal) for 90 d. RESULTS: The women were in positive copper balance only when the diet provided 47.2 micromol (3 mg) Cu and 811 micromol (53 mg) Zn/d. Immunoreactive ceruloplasmin concentrations and platelet cytochrome-c oxidase activity on a platelet number basis were significantly lower and the ratio between enzymatic and immunoreactive ceruloplasmin was significantly higher during low dietary than during high dietary zinc intake. Serum cholesterol was higher in subjects fed 15.7 micromol (1 mg) Cu/d than in those fed 47.2 micromol (3 mg) Cu/d. Total and low-density lipoprotein cholesterol concentrations decreased with zinc supplementation. Whole-blood glutathione concentration and erythrocyte glutathione peroxidase activity were lower during high than during low dietary zinc intake. CONCLUSIONS: The findings indicate that an inadequate intake of zinc (45.9 micromol/d; 3 mg/d) was more effective than a moderately high intake of zinc (811 micromol/d; 53 mg/d) in inducing changes associated with a decreased copper status in postmenopausal women. Furthermore, the findings indicate that copper status indicators might be useful in evaluating changes in zinc status in humans, and an intake of 15.7 micromol (1 mg)/d of copper may be inadequate for postmenopausal women.

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The effect of dietary sulfur amino acids on bioelectric properties was studied in rats by using bioimpedance spectroscopy. Weanling rats were assigned to one of 12 groups in a factorially arranged experiment with dietary variables of supplemental sulfur amino acid (none, 10 g DL-methionine/kg or 10 g DL-homocystine/kg), pyridoxine hydrochloride (0 or 7.5 mg/kg) and nickel (0 or 1 mg/kg). After 9 wk of feeding, 20-h urine specimens were collected from food-deprived rats for measurements of creatinine, and then bioimpedance was measured with multifrequency (Hydra ECF/ICF 4200) and single-frequency (RJL Systems model 101) analyzers. Urinary creatinine excretion was measured by intracellular water (ICW), total body solid and urinary volume (R2 = 0.675). Extracellular water (ECW) did not add significantly to the model. Rats fed methionine had significantly lower total body water, ICW and ECW than rats fed no supplemental sulfur amino acid. Rats fed homocystine had significantly lower ECW and a significantly higher ratio of ICW to ECW. Rats fed methionine or homocystine had significantly lower capacitance corrected for body length and ICW than those fed no supplemental sulfur amino acids. These results suggest that dietary homocystine changes the distribution of body water and that sulfur amino acids can affect membrane porosity and/or membrane thickness.

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Two experiments were conducted to determine effects of dietary boron (B) on performance, plasma minerals and metabolites, and bone characteristics in young pigs. In Experiment 1, 48 pigs (24 males, 24 females; 21 d old) were allotted to pens, which were randomly assigned to one of the following dietary treatments: 1) control (natural ingredient diet; 6.7 mg B/kg diet), 2) control + 5 mg B/kg diet and 3) control + 15 mg B/kg diet. Boron was supplemented as sodium borate. In Experiment 2, 48 pigs (24 males, 24 females; 21 d old) were assigned to the same treatments described in Experiment 1; however, the basal diet was a semipurified diet (0.98 mg B/kg diet). Diets were fed for 40 d; on d 40, blood samples were obtained for determination of plasma mineral and metabolite concentrations. Femurs were harvested from 8 pigs per treatment on d 40 for determination of mechanical properties, ash and lipid percentage. In Experiment 1, B did not affect performance, plasma minerals or metabolites or bone properties. In Experiment 2, B supplementation improved (P: < 0.05) the gain:feed ratio and increased plasma cholesterol and triglyceride concentrations. There was a treatment x sex interaction (P: < 0.05) in Experiment 2 for bone lipid to be lower and bending moment to be higher, with the response occurring in male pigs. Other dependent variables in Experiment 2 were not affected by treatment. In conclusion, B supplementation of a low B diet elicited responses of physiologic importance to pigs. However, B supplementation of a natural ingredient diet did not elicit a response.

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The environment in which living organisms evolved was apparently a primary determinant of which elements became essential for life. The first organic materials and, ultimately, life forms most likely were formed in an ancient sea containing minerals that provided structural integrity and catalytic ability to the first complex organic substances. The site at which life began has been suggested to be at the edge of the sea near sediments, or around a hydrothermal system. The strongest circumstantial evidence supports a hyperthermophilic beginning. Regardless of the site, the biological importance of elements tends to parallel oceanic abundance, but in higher forms of life this parallelism apparently has been mitigated by a natural selection process that resulted in some elements becoming more important because of their superior abilities over other elements to perform vital functions. The converse to biological importance is that toxicity of elements and oceanic abundance tends to be inversely related. The basis for this relationship may be that the efficiency of homeostatic mechanisms to cope with a high intake of a specific element probably reflects upon the exposure of an organism to the element during its evolution. Thus, a study of evolutionary events may be helpful in predicting and comprehending the essential and toxic nature of mineral elements in humans.

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Functional Electrical Stimulation (FES) is a controlled use of electrical stimulation of muscle contractions to obtain function. FES is utilised today in the treatment of spinal cord injured individuals for diaphragmatic pacing, bladder and bowel management, ejaculation, walking and hand function, as well as conditioning. We present The Freehand System, which consists of implanted electrodes to arm and hand muscles. This system has now been implanted in the first two Nordic tetraplegics. Candidates are tetraplegics with C5-6 lesions. After implantation it may take 6-8 months before the tetraplegic person can expect to use The Freehand System completely in daily life. The tetraplegic individual can choose between two grasps. The Freehand System can for some few very physically disabled tetraplegics be a good aid to increase their level of activities of daily living and independence. Continued development in the coming years may broaden the indications with benefit for more individuals.

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BACKGROUND: Zinc is an essential trace element for human health and well-being; however, methods currently available for the assessment of zinc status in humans are unsatisfactory. OBJECTIVE: The objective was to critically evaluate the use of various indicators of zinc status in humans in a controlled metabolic ward study. DESIGN: Indicators of zinc status were measured in 25 healthy postmenopausal women aged 64.9 +/- 6.7 y. After a 10-d equilibration period, volunteers consumed a diet with either a low (1 mg/d; n = 12) or a high (3 mg/d; n = 13) copper content based on a total energy content of 8.4 MJ. They received the same amount of copper throughout the study. Both groups were fed the basal diet (3 mg Zn/d) with no zinc supplement for one 90-d period, and the diet supplemented with 50 mg Zn/d for another 90-d period. RESULTS: Zinc supplementation significantly increased (P < 0.0001) extracellular but not erythrocyte superoxide dismutase activity. This increase was more apparent when subjects were fed the low-copper diet. Zinc supplementation in combination with the low-copper diet significantly decreased (P < 0.01) amyloid precursor protein expression in platelets. Other indicators of zinc status that were significantly elevated after zinc supplementation were as follows: plasma zinc and free thyroxine concentrations and mononuclear 5'-nucleotidase activity. CONCLUSION: The measurement of serum extracellular superoxide dismutase activity may be useful as a marker for the functional assessment of zinc status in humans.

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OBJECTIVE: Studies with rats have found that an interaction between fructose and magnesium affects macromineral metabolism; high dietary fructose significantly increased kidney calcification in both male and female rats, particularly when dietary magnesium was low. This study tests the hypothesis that an interaction between dietary fructose and magnesium adversely affects macromineral homeostasis in men. METHODS: Eleven men aged 22 to 40 years were fed a mixed, Western diet for four 42-day dietary periods in which dietary magnesium was either approximately 170 or 370 mg/day and dietary fructose was either 4% or 20% of energy. A decaffeinated beverage containing high fructose corn syrup replaced cornstarch, bread and rice in the low fructose diet to give the high fructose diet. RESULTS: High dietary fructose significantly (p<0.01) increased magnesium balance during both low and high dietary magnesium intakes. Ultrafilterable and ionized serum magnesium also apparently were related to magnesium and fructose intakes; they were higher when fructose was fed and when Mg intakes were high. High fructose depressed calcium balance: the effect tended to be more marked when dietary Mg was low. High dietary fructose also significantly (p<0.005) decreased phosphorous balance. Urinary phosphorous losses were significantly (p<0.001) higher when high dietary fructose was fed. High dietary fructose also increased the concentration of serum alkaline phosphatase (p<0.005). CONCLUSION: These findings indicate that dietary fructose adversely affects macromineral homeostasis in humans and suggest further studies to see if a high fructose diet coupled with low dietary magnesium and marginal calcium leads to bone loss.

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Larvae of Coccinella septempunctata were reared on three aphid diets, consisting of pure Rhopalosiphum padi, pure Metopolophium dirhodum, and an equal mix of these aphid species. In the pupal stage, the activities of three detoxifying enzyme systems - glutathione S-transferase (GST) with 1-chloro-2,4-dinitrobenzene as substrate, glutathione peroxidase with hydrogen peroxide as substrate (GSH-Px[H2O2]), and glutathione peroxidase with tert-butyl hydroperoxide as substrate (GSH-Px[TBH]) - were assayed. Growth rate, measured as the total protein content of the pupae, was significantly higher in the mixed-diet group than in the R. padi group, whereas that of the M. dirhodum group was intermediate. GST showed lower activity in larvae on a pure R. padi diet and a mixed aphid diet than on a pure M. dirhodum diet, whereas the variation in GSH-Px[TBH] was independent of diet. GSH-Px(H2O2) showed a significantly higher activity in the R. padi group than in the M. dirhodum group, whereas that of the mixed-diet group was intermediate. Thus, feeding on the low-quality aphid, R. padi, inhibited GST and activated GSH-Px(H2O2). The induction of GSH-Px[H2O2] indicated elevated oxidative stress. This may have been caused by toxic compounds in the R. padi.

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To date, boron (B) essentiality has not been conclusively shown in mammals. This article summarizes the results of a series of in vitro and in vivo experiments designed to investigate the role of B in mammalian reproduction. In the first study, rat dams were fed either a low (0.04 microg B/g) or an adequate (2.00 microg B/g) B diet for 6 wk before breeding and through pregnancy; reproductive outcome was monitored on gestation day 20. Although low dietary B significantly lowered maternal blood, liver, and bone B concentrations, it had no marked effects on fetal growth or development. The goal of the second study was to assess the effects of B on the in vitro development of rat postimplantation embryos. Day 10 embryos collected from dams fed either the low or adequate B diets for at least 12 wk were cultured in serum collected from male rats exposed to one of the two dietary B treatments. Dams fed the low B diet had a significantly reduced number of implantation sites compared to dams fed the B-adequate diet. However, embryonic growth in vitro was not affected by B treatment. The aim of study 3 was to define the limits of boric acid (BA) toxicity on mouse preimplantation development in vitro. Two-cell mouse embryos were cultured in media containing graded levels of BA (from 6 to 10,000 microM). Impaired embryonic differentiation and proliferation were observed only when embryos were exposed to high levels of BA (>2000 microM), reflecting a very low level of toxicity of BA on early mouse embryonic development. Study 4 tested the effects of low (0.04 microg B/g) and adequate (2.00 microg B/g) dietary B on the in vitro development of mouse preimplantation embryos. Two-cell embryos obtained from the dams were cultured in vitro for 72 h. Maternal exposure to the low B diet for 10, 12, and 16 wk was associated with a reduction in blastocyst formation, a reduction in blastocyst cell number, and an increased number of degenerates. Collectively, these studies support the concept that B deficiency impairs early embryonic development in rodents.

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Because a biochemical function has not been defined for boron (B), its nutritional essentiality has not been firmly established. Nonetheless, dietary guidance should be formulated for B, because it has demonstrated beneficial, if not essential, effects in both animals and humans. Intakes of B commonly found with diets abundant in fruits, vegetables, legumes, pulses, and nuts have effects construed to be beneficial in macromineral, energy, nitrogen, and reactive oxygen metabolism, in addition to enhancing the response to estrogen therapy and improving psychomotor skills and cognitive processes of attention and memory. Perhaps the best-documented beneficial effect of B is on calcium (Ca) metabolism or utilization, and thus, bone calcification and maintenance. The paradigm emerging for the provision of dietary guidance that includes consideration of the total health effects of a nutrient, not just the prevention of a deficiency disease, has resulted in dietary guidance for chromium (Cr) and fluoride; both of these elements have beneficial effects in humans, but neither has a defined biochemical function. Knowledge of B nutritional effects in humans equals or is superior to that of Cr and fluoride; thus, establishing a dietary reference intake for B is justified. An analysis of both human and animal data suggests that an acceptable safe range of population mean intakes of B for adults could well be 1-13 mg/d. Recent findings indicate that a significant number of people do not consistently consume more than 1 mg B/d; this suggests that B could be a practical nutritional or clinical concern.

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Findings from animal studies indicate that dietary boron affects several aspects of mineral metabolism, especially when animals are subjected to nutritional stressors. Eleven postmenopausal volunteers living on a metabolic ward for 167 d (one 23-d equilibration period and six 24-d treatment periods) were fed a conventional basal diet that supplied a daily average intake of 0.36 mg B, 109 mg Mg, and < 0.10 mg A1/8400 kJ. They were given supplements of 0 (BB) or 3 mg B (SB, last two periods only), 0 (BMg) or 200 mg Mg (SMg) (with magnesium supplements held constant during the last two periods), or 0 (BAl) or 1000 mg A1 (SAl)/d. The SB treatment, compared with the BB treatment, provided a 9.0-fold increase in dietary boron but yielded only a 1.5-fold increase in plasma boron concentrations. Regardless of boron dietary treatment, fecal plus urinary excretion of boron accounted for nearly 100% of dietary boron intake with no evidence of boron accumulation over time. Lack of boron accumulation and relatively small changes in blood boron values during a substantial increase in dietary boron support the concept of boron homeostasis. In subjects fed BMg, SB decreased the percentage of dietary calcium lost in the urine but increased that percentage in volunteers fed SMg, a relation that may be important in understanding metabolic mineral disorders that perturb calcium balance. Reduced calcium absorption during SAl suggests that aluminum supplementation should be limited or at least monitored in postmenopausal women prone to excessive calcium loss. Decreased total urinary oxalate during SB in BMg subjects indicates a possible role for boron in the control of urolithiasis during low-magnesium nutriture.

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The term ultratrace elements, often used to indicate elements with an established, estimated or suspected requirement generally indicated by microgram/, could be applied to at least 20 elements. The quality of experimental evidence for nutritional essentiality varies widely for the ultratrace elements. Thus, although differing dietary guidance is appropriate for these elements, most need increased attention in future editions of the Recommended Dietary Allowances (RDAs) for the following reasons: (1) Increased interest in these elements by the public has been stimulated by the mass media; thus, responsible information about the usefulness of the ultratrace elements for health and well being is needed. (2) Risk assessments and toxicological standards are influenced by the RDAs. Authorative advice is required to prevent standards that obstruct the achievement of beneficial intakes of ultratrace elements. (3) An emerging new paradigm is that the determination of nutritional requirements should include consideration of the total health effects of nutrients, not just their roles in preventing deficiency pathology; some of the ultratrace elements have identified health benefits. Six ultratrace elements, iodine, selenium, manganese, molybdenum, chromium and boron (and cobalt as vitamin B12), merit specific RDAs. The term "estimated safe and adequate daily dietary intakes (ESADDI)" should not be used for any of the other ultratrace elements because of the misleading words "adequate" and "safe". "Apparent beneficial intake (ABI)" seems more appropriate for the elements with beneficial, if not essential, actions that can be extrapolated from animals to humans; these elements include arsenic, fluoride, lithium, nickel, silicon and vanadium. The evidence is too limited or controversial for the remaining ultratrace elements to even provide an ambiguous ABI. The amount found in a healthful diet probably should be a value provided for an appropriate intake for aluminum, bromide, cadmium, germanium, lead, rubidium, and tin.

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