Dietary selenium intake modulates thyroid hormone and energy metabolism in men

Most studies of selenium and thyroid hormone have used sodium selenite in rats. However, rats regulate thyroid hormone differently, and selenite, which has unique pharmacologic activities, does not occur in foods. We hypothesized that selenium in food would have different effects in humans. Healthy men were fed foods naturally high or low in selenium for 120 d while confined to a metabolic research unit. Selenium intake for all subjects was 47 microg/d (595 nmol/d) for the first 21 d, and then changed to either 14 (n = 6) or 297 (n = 5) microg/d (177 nmol/d or 3.8 micromol/d) for the remaining 99 d, causing significant changes in blood selenium and glutathione peroxidase. Serum 3,3',5-triiodothyronine (T3) decreased in the high selenium group, increased in the low selenium group, and was significantly different between groups from d 45 onward. A compensatory increase of thyrotropin occurred in the high selenium group as T3 decreased. The changes in T3 were opposite in direction to those reported in rats, but were consistent with other metabolic changes. By d 64, the high selenium group started to gain weight, whereas the low selenium group began to lose weight, and the weight changes were significantly different between groups from d 92 onward. Decreases of serum T3 and compensatory increases in thyrotropin suggest that a subclinical hypothyroid response was induced in the high selenium group, leading to body weight increases. Increases of serum T3 and serum triacylglycerol accompanied by losses of body fat suggest that a subclinical hyperthyroid response was induced in the low selenium group, leading to body weight decreases.     

Molybdenum kinetics in men differ during molybdenum depletion and repletion

In this study we developed an expanded compartmental model of molybdenum (Mo) kinetics to determine rates of molybdenum distribution during molybdenum depletion and repletion. The model was based on a clinical study in which 4 men consumed a low-molybdenum diet of 22 microg/d (0.23 micromol/d) for 102 d, followed by a high molybdenum diet of 467 microg/d (4.9 micromol/d) for 18 d. Stable isotopes 100Mo and 97Mo were administered orally and intravenously, respectively, at several time points during the study, and serial samples of plasma, urine, and feces were analyzed for 100Mo, 97Mo, and total Mo. Based on plasma, urine, and fecal molybdenum levels, kinetic parameters of distribution and elimination were determined. The rates of molybdenum distribution and elimination were different during depletion and repletion. During high intake, urinary molybdenum excretion was greater than during low intake. In addition, fractional tissue storage of molybdenum was lower during high intake than during low intake. This suggests that low intake results in an adaptation to conserve body Mo, and that high intake results in an adaptation to eliminate Mo. The model also suggested that food-bound molybdenum was approximately 16% less bioavailable than purified Mo. Finally, under the conditions of this study, the model suggested that an intake of 43 microg/d (0.45 micromol/d) would be sufficient to maintain plasma molybdenum levels at steady state. This is a minimum estimate because subjects in this study were in a molybdenum-sparing state. These findings provide an understanding of the adaptations in molybdenum metabolism that take place during depletion and repletion.     

A moderately high intake compared to a low intake of zinc depresses magnesium balance and alters indices of bone turnover in postmenopausal women

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.     

Selenium and zinc status are suboptimal in a sample of older New Zealand women in a community-based study

The importance of selenium and zinc in the immune functioning of the aged is widely recognized. Seniors in New Zealand are at particularly high risk of low selenium status because of the low selenium soil environment. The zinc status of the New Zealand elderly has never been assessed. In this cross-sectional study, the biochemical selenium, zinc and lipid levels, physical functional capacity and dietary intakes of 103 randomly selected free-living New Zealand women (mean age +/- SD, 75 +/- 3 y) were assessed. Among nonusers of selenium supplements (n = 80), 80% [95% confidence interval (CI): 70; 88%] had plasma selenium levels (0.85 +/- 0.23 micromol/L) below 1.00 micromol/L [ approximately 10% below mean plasma selenium necessary for full expression of glutathione peroxidase (GPx) activity in New Zealand subjects]. Plasma selenium was strongly correlated with GPx: r = 0.56; P < 0.0001. For nonusers of zinc supplements (n = 88), serum zinc concentrations were 12.4 +/- 1.4 micromol/L, with 12% (95% CI: 6; 21%) having levels below the cut-off value (10.7 micromol/L). Estimated mean daily selenium and zinc intakes were 34 +/- 10 microg and 8.7 +/- 2.0 mg, respectively. Subjects in the highest tertile of a functional capacity index had higher biochemical zinc and selenium values than those in the lowest tertile (P < 0.05). The correlation between plasma selenium and GPx indicates that selenium intake in these women is still insufficient for full expression of GPx activity. Lower serum zinc levels also appear to be prevalent. Because a suboptimal trace element status may be more common among those with a poor physical functioning, promotion of the consumption of nutrient dense foods or supplements to improve selenium and zinc status of elderly women in New Zealand may be beneficial.     

Metallothionein in mice reduces intestinal zinc loss during acute endotoxin inflammation, but not during starvation or dietary zinc restriction

Normal metallothionein [(MT)+/+] and MT-null (MT-/-) mice were used to examine the influence of MT on Zn retention and the metabolic consequences of 2 d food deprivation, with and without inflammation induced by intraperitoneal injection of bacterial endotoxin lipopolysaccharide (LPS). LPS reduced fecal Zn concentration in MT+/+ mice from 5.9 +/- 0.2 micromol/g on d 1 to 2.2 +/- 0.2 micromol/g on d 2, but not in MT-/- mice, 5.9 +/- 0.2 and 5.7 +/- 0. 5 micromol/g, respectively. MT+/+ mice fed an 8 mg Zn/kg diet and injected with LPS excreted 40% less Zn over 2 d than their MT-/- counterparts. Starvation for 2 d did not lower fecal Zn concentration in either genotype, although in MT+/+ mice, urinary Zn excretion was reduced from 12.7 +/- 1.3 nmol on d 1 to 5.9 +/- 1.8 nmol on d 2 and plasma Zn concentration was lowered to 9.8 +/- 0.4 micromol/L. Zn was not reduced in urine or plasma of MT-/- mice, with respective values of 10.8 +/- 2.0 nmol on d 1, 9.3 +/- 2.9 nmol on d 2 and 13.0 +/- 1.0 micromol/L. LPS injection resulted in much higher total liver Zn (677 +/- 27 nmol) and MT (106 +/- 2 nmol Cd bound/g) than starvation (Zn = 405 +/- 21, MT = 9 +/- 3) in MT+/+ mice after 2 d, but did not further reduce urinary Zn. LPS-injected MT-/- mice had no rise in liver Zn or fall in plasma and urine Zn. MT-/- mice fed a Zn-deficient (0.8 mg Zn/kg) diet lost 10% of body weight over 25 d compared with no loss in MT+/+ mice. Despite this, MT-/- mice excreted no more Zn via the gut than did MT+/+ mice. In summary, MT inhibits intestinal Zn loss when highly expressed. When uninduced, typically during Zn deficiency, MT appears to conserve Zn and body mass by reducing only urinary and other nonintestinal Zn losses.     

Folate intake at RDA levels is inadequate for Mexican American men with the methylenetetrahydrofolate reductase 677TT genotype

Since the establishment of the 1998 folate recommended dietary allowance (RDA), the methylenetetrahydrofolate reductase (MTHFR) 677C-->T variant has emerged as a strong modifier of folate status. This controlled feeding study investigated the adequacy of the RDA, 400 microg/d as dietary folate equivalents (DFE), for Mexican American men with the MTHFR 677CC or TT genotype. Because of the interdependency between folate and choline, the influence of choline intake on folate status was also assessed. Mexican American men (n = 60; 18-55 y) with the MTHFR 677CC (n = 31) or TT (n = 29) genotype consumed 438 microg DFE/d and total choline intakes of 300, 550 (choline adequate intake), 1100, or 2200 mg/d for 12 wk. Folate status response was assessed via serum folate (SF), RBC folate, plasma total homocysteine (tHcy), and urinary folate. SF decreased (P < 0.001) 66% to 7.9 +/- 0.7 nmol/L (means +/- SEM) in men with the 677TT genotype and 62% to 11.3 +/- 0.9 nmol/L in the 677CC genotype. Plasma tHcy increased (P < 0.0001) 170% to 31 +/- 3 micromol/L in men with the 677TT genotype and 18% to 11.6 +/- 0.3 micromol/L in the 677CC genotype. At the end of the study, 34% (677TT) and 16% (677CC) had SF concentrations <6.8 nmol/L and 79% (677TT) and 7% (677CC) had tHcy concentrations >14 micromol/L. Choline intake did not influence the response of the measured variables. These data showed that the folate RDA is not adequate for men of Mexican descent, particularly for those with the MTHFR 677TT genotype, and demonstrated a lack of influence of choline intake on the folate status variables measured in this study.     

Selenate-supplemented nutritional formula increases plasma selenium in hemodialysis patients.

OBJECTIVE: The purpose of this study was to determine the short-term effect of feeding selenium-supplemented formulas on the selenium status of end-stage renal disease patients on hemodialysis. DESIGN AND SETTING: The prospective, randomized, single-blind study of parallel design was conducted at three hemodialysis clinics. PATIENTS: A total of 79 hemodialysis patients were randomly assigned into one of three groups. INTERVENTION: Liquid nutritional formula supplemented with either selenite (28 microg Se/8 oz, n = 26), selenate (28 microg Se/8 oz, n = 26), or nonfortified (7 microg Se/8 oz, n = 27) was fed to hemodialysis patients as their sole source of nutrition for 14 days. MAIN OUTCOME MEASURE: Plasma and red blood cell (RBC) selenium and glutathione peroxidase (GPX) activities were measured in predialysis blood both before (day 1) and after (day 8) a 7-day baseline period, and after subjects received the formula as the sole source of nutrition (approximately 35 kcal/kg/d) for 14 days (day 22). RESULTS: Selenium intake (Mean +/- SEM, microg/d) was 134 +/- 9, 140 +/- 9, and 35 +/- 2 for patients receiving selenite-, selenate-, or non-supplemented formula, respectively. On day 22, plasma selenium (micromol/L) was greater (P <.032) in the selenate-supplemented group (1.5 +/- 0.1) compared with the nonsupplemented group (1.2 +/- 0.1), but not compared with the selenite-supplemented group (1.4 +/- 0.1). Plasma GPX activity was 44% to 60% that of healthy controls and not different among groups. RBC selenium and GPX activities were within the normal range and were not different among groups. CONCLUSION: The results of this study indicate that a liquid formula supplemented with selenium as selenate is successful at maintaining selenium concentrations within normal range, as well as significantly increasing plasma selenium levels compared with nonsupplementation.     

Low dietary zinc alters indices of copper function and status in postmenopausal women

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.     

Effect of the methylenetetrahydrofolate reductase 677C-->T mutation on the relations among folate intake and plasma folate and homocysteine concentrations in a general population sample

BACKGROUND: Methylenetetrahydrofolate reductase (MTHFR) is a key enzyme in folate and homocysteine metabolism. The common MTHFR 677C-->T polymorphism decreases the enzyme's activity. OBJECTIVE: The objective of the study was to assess the effect of the polymorphism on the relations among folate intake, plasma folate concentration, and total plasma homocysteine (tHcy) concentration. DESIGN: The design was a cross-sectional analysis in a random sample (n = 2051) of a Dutch cohort (aged 20-65 y). RESULTS: At a low folate intake (166 micro g/d), folate concentrations differed significantly among the genotypes (7.1, 6.2, and 5.4 nmol/L for the CC, CT, and TT genotypes, respectively; P for all comparisons < 0.05). At a high folate intake (250 microg/d), folate concentrations in CT and CC subjects did not differ significantly (8.3 and 8.6 nmol/L, respectively, but were significantly higher (P = 0.2) than those in TT subjects (7.3 nmol/L; P = 0.04). At a low folate concentration (4.6 nmol/L), TT subjects had a significantly higher (P = 0.0001) tHcy concentration than did CC and CT subjects (20.3 compared with 15.0 and 14.1 micromol/L, respectively), whereas at a high folate concentration (11.9 nmol/L), the tHcy concentration did not differ significantly between genotypes (P > 0.2; <13.1 for all genotypes). The relation between folate intake and tHcy concentration had a pattern similar to that of the relation between plasma folate and tHcy concentrations. CONCLUSIONS: At any folate intake level, TT subjects have lower plasma folate concentrations than do CT and CC subjects. Yet, at high plasma folate concentrations, tHcy concentrations in TT subjects are as low as those in CT and CC subjects.     

Glutathione blood levels and other oxidant defense indices in men fed diets low in vitamin C

Because ascorbic acid is an important contributor to the oxidant defense system in body tissues, we studied the effects of a low dietary intake of ascorbic acid on various indicators of oxidant defense and oxidant damage. During a 13-wk study eight healthy men (25-43 y), residing in a live-in metabolic unit, were fed controlled diets containing different amounts of ascorbic acid for four consecutive periods: period 1 = 250 mg/d for 4 d; period 2 = 5 mg/d for 32 d; period 3 = 10 or 20 mg/d for 28 d and period 4 = 60 or 250 mg/d for 28 d. Measurements were made at several time intervals of the activities of glutathione peroxidase and superoxide dismutase in RBC, DNA strand breaks in mononuclear leucocytes, glutathione concentrations in plasma and RBC and NAD and NADP in RBC. After 60 d of low ascorbic acid intakes and associated with plasma ascorbic acid levels less than 6 mumol/L, the total glutathione concentration and the reduced glutathione:oxidized glutathione ratio were decreased in plasma. At the same time NAD and NADP levels in RBC were elevated. It seems that chronic marginal vitamin C deficiency states may be associated with selected biochemical changes in oxidant defense indices.     

Molybdenum intake influences molybdenum kinetics in men

The objectives of this study were to determine physiologic adaptations that occur when humans are exposed to a wide range of molybdenum intake levels and to identify the pathways that are influenced by dietary intake. Four males consumed each of 5 daily molybdenum intakes of 22, 72, 121, 467, and 1490 microg/d (0.23, 0.75, 1.3, 4.9, and 15.5 micromol/d) for 24 d each. During each treatment period, oral and intravenous doses of (100)Mo and (97)Mo were administered. Serial plasma, urine, and fecal samples were analyzed for labeled and unlabeled molybdenum. Compartmental modeling was used to determine rates of distribution and elimination at each dietary intake level. Three pathways were sensitive to daily molybdenum intake. With increasing intake, absorption and urinary molybdenum excretion increased, whereas the fraction deposited in tissues decreased. Kinetic analysis suggested a daily intake of 115-120 microg/d (1.20-1.25 micromol/d) would maintain initial plasma molybdenum levels at their prestudy values and that their prestudy dietary intake was well above the Recommended Dietary Allowance of 45 microg/d. The physiological adaptations to changing intake that the model demonstrated may help prevent molybdenum deficiency and toxicity.     

Trace element loss in urine and effluent following traumatic injury

BACKGROUND: Few data are available to establish recommendations for trace element supplementation during critical illness. This study quantified the loss of several elements and assessed the adequacy of manganese and selenium in parenteral nutrition (PN). METHODS: Men with traumatic injuries were grouped by renal status: adequate (POLY; n = 6), acute failure with continuous venovenous hemofiltration (CVVH; n = 2), or continuous venovenous hemodiafiltration (CVVHD; n = 4). PN supplied 300 microg/d manganese and 60 microg/d selenium. Urine and effluent (from artificial kidneys) were collected for 3 days and analyzed for boron, manganese, nickel, and silicon using inductively coupled plasma atomic emission spectrometry, and for selenium using atomic absorption spectrometry. RESULTS: POLY manganese and selenium excretion averaged (standard deviation [SD]) 7.9 (3.3) microg/d and 103.5 (22.4) microg/d, respectively. All elements except selenium were detected in dialysate (prior to use). CVVHD effluent contained 3.5 and 7.3 times more manganese and nickel than CVVH ultrafiltrate, respectively. Loss of manganese averaged 2.6%, 21%, and 73% of PN amounts for POLY, CVVH, and CVVHD groups, respectively. DISCUSSION: Minimal loss of manganese compared with the amount in PN suggests that excessive amounts are retained. POLY patients excreted more selenium than was in PN, indicating negative balance. POLY losses of boron and silicon were less than that published for healthy adults, reflecting less than typical intake, whereas loss during CVVH was in the normal reference range, possibly because of added intake from boron contamination of replacement fluids. All patients lost more nickel than amounts published for healthy adults. CONCLUSIONS: Current guidelines of 60-100 microg/d of parenteral manganese may be excessive for trauma patients. The uptake of manganese and nickel from contaminants in CVVHD dialysate should be investigated.     

Association between B vitamin intake and plasma homocysteine concentration in the general Dutch population aged 20-65 y

BACKGROUND: An elevated plasma total homocysteine (tHcy) concentration is associated with an increased risk of cardiovascular diseases. Folate, riboflavin, vitamin B-6, and vitamin B-12 are essential in homocysteine metabolism. OBJECTIVE: The objective was to describe the association between dietary intakes of folate, riboflavin, vitamin B-6, and vitamin B-12 and the nonfasting plasma tHcy concentration. DESIGN: A random sample of 2435 men and women aged 20-65 y from a population-based Dutch cohort examined in 1993-1996 was analyzed cross-sectionally. RESULTS: Univariately, intakes of all B vitamins were inversely related to the plasma tHcy concentration. In multivariate models, only folate intake remained inversely associated with the plasma tHcy concentration. Mean plasma tHcy concentrations (adjusted for intakes of riboflavin, vitamin B-6, vitamin B-12, and methionine and for age, smoking, and alcohol consumption) in men with low (first quintile: 161 microg/d) and high (fifth quintile: 254 microg/d) folate intakes were 15.4 and 13.2 micromol/L, respectively; in women, plasma tHcy concentrations were 13.7 and 12.4 micromol/L at folate intakes of 160 and 262 microg/d, respectively. In men, the difference in the mean plasma tHcy concentration between men with low and high folate intakes was greater in smokers than in nonsmokers (2.8 compared with 1.6 micromol/L) and greater in nondrinkers than in drinkers of >2 alcoholic drinks/d (3.5 compared with 1.4 micromol/L). In women, the association between folate intake and plasma tHcy was not modified by smoking or alcohol consumption. CONCLUSIONS: In this Dutch population, folate was the only B vitamin independently inversely associated with the plasma tHcy concentration. Changing dietary habits may substantially influence the plasma tHcy concentration in the general population.     

Kinetics of folate turnover in pregnant women (second trimester) and nonpregnant controls during folic acid supplementation: stable-isotopic labeling of plasma folate, urinary folate and folate catabolites shows subtle effects of pregnancy on turnover of folate pools.

To investigate the effects of pregnancy on folate metabolism, we conducted an 84-d study in second-trimester (gestational wk 14-25) pregnant women (n = 6) and nonpregnant controls (n = 6) with stable-isotopic tracer methods. All subjects were fed a diet containing approximately 272 nmol/d (120 microg/d) folate from food, along with supplemental folic acid that contained 15% [3',5'-(2)H(2)] folic acid ([(2)H(2)]folic acid) during d 1--41 and that was unlabeled during d 42--84 to yield a constant total folate intake of 1.02 or 1.93 micromol/d (450 or 850 microg/d). Isotopic enrichment of plasma folate, urinary folate and the urinary folate catabolites para-aminobenzoylglutamate (pABG) and para-acetamidobenzoylglutamate (ApABG) was determined at intervals throughout the study. The labeling of pABG and ApABG reflected that of tissue folate pools from which the catabolites originate. After the intake of labeled folic acid was terminated on d 41, labeling of urinary folate exhibited a biphasic exponential decline with distinct fast and slow components. In contrast, during d 42--84, the enrichment of urinary pABG and ApABG exhibited primarily monophasic exponential decline, and plasma folate underwent little decline of labeling during this period. Pregnant women and controls did not differ in estimates of body folate pool size and most aspects of the excretion of labeled urinary folate and catabolites, rates of decline of excretion, and areas under the curves for folate and catabolite excretion. Pregnant women, however, tended to have a slower rate of decline of pABG than ApABG and higher enrichment at d 42 of ApABG and pABG. These data support and extend our previous findings indicating that pregnancy (gestational wk 14--26) causes subtle changes in folate metabolism but does not elicit substantial increases in the rate or extent of folate turnover at these moderately high folate intakes.     

Long-term high copper intake: effects on copper absorption, retention, and homeostasis in men

BACKGROUND: Numerous studies have examined the effect of low and adequate intakes of copper on absorption and retention, but little information is available on the regulation of absorption and retention of copper when intake is high. OBJECTIVE: A study was conducted in men to determine the effect of long-term high copper intake on copper absorption, retention, and homeostasis. DESIGN: Nine men were confined to a metabolic research unit (MRU) for 18 d and were fed a 3-d rotating menu containing an average of 1.6 mg Cu/d. They continued the study under free-living conditions for 129 d, supplementing their usual diets with 7 mg Cu/d. They then returned to the MRU for 18 d and consumed the same diet as during the first period, except that copper intake was 7.8 mg/d. The stable isotope (63)Cu was fed to 3 subjects and infused into the other 6 on day 7 of each MRU period, and complete urine and stool collections were made throughout the study. Total copper and (63)Cu were determined by inductively coupled plasma mass spectrometry. Copper absorption, excretion, and retention were calculated on the basis of dietary, urinary, and fecal copper and (63)Cu. RESULTS: Results were as follows when comparing the high copper intake with the usual intake: fractional copper absorption was significantly lower, but the amount absorbed was significantly higher; excretion of the infused (63)Cu was significantly faster; and total retention was significantly higher. CONCLUSIONS: Homeostatic regulation of copper absorption and retention helped to minimize the amount of copper retained with high copper intake but was not sufficient to prevent retention of >0.6 mg Cu/d.     

Selenium intakes,absorption, retention,and status in adolescent girls

OBJECTIVES: To assess selenium intakes, absorption, retention, and status in healthy adolescent girls and the effect of calcium supplementation on selenium parameters. DESIGN: Annual 2-week study conducted each year for 3 consecutive years in which yearly selenium intakes, absorption, and retention and blood selenium status were measured. SETTING: A metabolic unit in a large metropolitan hospital located in Columbus, Ohio--a low selenium region of the United States. SUBJECTS: Healthy white girls aged 11 to 14 years (n=16) enrolled in a calcium balance study and randomly assigned to receive a placebo of methylcellulose (n=9) or a calcium supplement containing 1,000 mg supplemental calcium as calcium citrate malate (n=7). INTERVENTIONS: Each subject consumed a diet with approximately 100 microg selenium/day during the yearly 2-week balance studies. RESULTS: Selenium status measurements (serum and erythrocyte selenium and glutathione peroxidase activity) were all within normal ranges for adults during the study. Apparent selenium absorption averaged 71%, 76%, and 74% for years 1, 2, and 3 of the study, respectively, and did not vary significantly (P>.05). Average daily selenium retention did not differ among the years of the study (P>.05) and indicated that the usual selenium intake was approximately 100 microg daily. Measurements of selenium status and retention did not differ between calcium-supplemented and placebo groups. CONCLUSIONS: An intake of approximately 100 microg selenium/day is the typical intake of the mineral among the subjects and appeared adequate to maintain selenium status in these healthy adolescent girls; in addition, calcium supplementation of 1,000 mg daily does not have a negative impact on selenium parameters.     

Evaluation of folate status by serum and erythrocyte folate levels and dietary folate intake in Taiwanese schoolchildren

The folate status and dietary folate intake of Taiwanese schoolchildren was investigated by analysis of both serum and red blood cell (RBC) folate levels and dietary folate intake in 1105 boys and 958 girls aged 6-13 years sampled from the Nutrition and Health Survey in Taiwan Elementary School Children 2001-2002 (NAHSIT Children 2001-2002). Mean serum folate levels were 18.3+/-8.8 nmol/L (8.1+/-3.9 ng/mL) in boys and 20.3+/-9.7 nmol/L (9.0+/-4.3 ng/mL) in girls. Mean RBC folate levels were 700+/-320 nmol/L (308+/-141 ng/mL) in boys and 751+/-347 nmol/L (331+/-153 ng/mL) in girls. The prevalence of serum folate deficiency was 1.4% in boys and girls, and the prevalence of marginal serum folate deficiency (7-14 nmol/L) was 31.1% in boys and 25.8% in girls. In addition, 8.5% of boys and 7.4% girls had RBC folate deficiency (RBC folate < 318 nmol/L), and 17% of children had marginal RBC folate deficiency (RBC folate of 318-454 nmol/L). Our results suggesting that Taiwanese schoolchildren have poor folate status especially during periods of rapid growth and development such as the transition from childhood to early adolescence (boys at age 12-12.9, girls at age 11-12.9). The average estimated folate intakes were 269+/-9 microg/d in boys and 259+/-9 microg/d in girls, and 42% of Taiwanese schoolchildren had a dietary folate intake below 2/3 of the RDA, indicating a poor dietary folate intake in this population. This study shows that the folate status of Taiwanese schoolchildren is currently inadequate and strategies are needed for improvement.     

Urinary excretion of folate catabolites responds to changes in folate intake more slowly than plasma folate and homocysteine concentrations and lymphocyte DNA methylation in postmenopausal women

Folate turnover involves urinary excretion, fecal excretion, and catabolism that involves cleavage of the C9-N10 bond to yield pterins and para-aminobenzoylglutamate (pABG). Little is known about the relationship between the function of folate pools and their rates of catabolism. We report here an investigation of excretion of urinary pABG and its primary excretory form, para-acetamidobenzoylglutamate (ApABG) in samples collected during a previously published study of postmenopausal women. Ten women (49-63 y) were fed a low folate diet (56 microg/d) supplemented with folic acid to yield total folate intakes of 195 microg/d (d 1-5), 56 microg/d (d 6-41), 111 microg/d (d 42-69), 286 microg/d (d 70-80) and 516 microg/d (d 81-91). This caused changes in plasma folate, plasma homocysteine and global methylation of lymphocyte DNA. For each subject, a 7-d pooled urine sample was collected over d 1-7, 36-42, 64-70 and 85-91. ApABG constituted >85% of total catabolite excretion, and folate intake did not significantly influence ApABG or pABG excretion. The molar ratio of total catabolite excretion/folate intake varied significantly, with ratios of 1.0 +/- 0.17 (d 1-7), 3.0 +/- 0.55 (d 36-42), 1.1 +/- 0.18 (d 64-70) and 0. 33 +/- 0.054 (d 85-91). These observations indicate that the rate of folate catabolite excretion is related mainly to masses of slow-turnover folate pools governed by long-term folate intake. Folate pools functioning in some forms of methyl group metabolism respond to dietary changes in folate intake much more rapidly.     

Copper deficiency does not lead to taurine deficiency in rats

Copper deficiency has been reported to cause a decrease in urinary taurine excretion in rats. We determined whether Cu deficiency would decrease taurine status and the hepatic activities of cysteine dioxygenase (CDO) and/or cysteine sulfinic acid decarboxylase (CSAD) in rats. Ten weanling male rats were assigned to either a Cu-adequate (+Cu) or Cu-deficient (-Cu) group. All rats consumed a Cu-deficient purified diet and water ad-libitum for 16 wk. The water for the (+Cu) group contained 20 mg Cu/L as CuSO(4). At wk 16, the groups differed (P < 0.05) in the following variables (means +/- SEM, -Cu vs. +Cu): body weight (BW), 375 +/- 19 vs. 418 +/- 2.9 g; food intake, 16.2 +/- 0.7 vs. 18.5 +/- 0.4 g/d; hematocrit, 0.294 +/- 0.027 vs. 0.436 +/- 0.027; hemoglobin, 95.2 +/- 9 vs 134 +/- 10 g/L; liver Cu, 8.7 +/- 2.0 vs. 65.9 +/- 2.5 nmol/g; plasma Cu, 0.38 +/- 0.09 vs. 13.4 +/- 0.61 micromol/L; plasma ceruloplasmin activity, 1.75 +/- 1.0 vs. 67.9 +/- 8.4 IU; relative heart weight, 0.56 +/- 0.04 vs. 0.35 +/- 0.02% BW; relative liver weight, 4.06 +/- 0.23 vs. 3.37 +/- 0.06% BW; and liver CSAD activity, 18.8 +/- 1.37 vs. 13.5 +/- 1.11 nmol x min(-1) x mg protein(-1). The groups did not differ at wk 16 in: plasma taurine, 249 +/- 14 vs. 298 +/- 63 micromol/L; whole blood taurine, 386 +/- 32 vs. 390 +/- 25 micromol/L; urinary taurine excretion, 82.5 +/- 15 vs. 52.0 +/- 8.3 micromol/d; liver taurine, 2.6 +/- 0.7 vs. 2.8 +/- 0.4 micromol/g; liver total glutathione, 6.9 +/- 0.48 vs. 6.3 +/- 0.40 micromol/g; liver cyst(e)ine, 96 +/- 7.1 vs. 99 +/- 5.3 nmol/g and liver CDO activity, 2.19 +/- 0.33 vs. 2.74 +/- 0.21 nmol x min(-1) x mg protein(-1). These findings support the conclusion that Cu deficiency does not affect body taurine status.     

Dietary habits and selenium intake of residents in mountain and coastal communities in Japan

We used a Simple Food Frequency Questionnaire (SFFQ) in combination with other dietary approaches to estimate the selenium intake from different food groups based on the average long-term diet, in two rural communities in Japan, one in a mountain area and the other in a coastal area. The intake frequencies of rice and wheat products were significantly different in the two districts. The intake frequencies of fish, meat, and eggs, which are rich in selenium, were not significantly different. The mean dietary selenium intake, estimated from the SFFQ and the 24-h recall method, was 82.7 microg/d (n=234) (range 19.2-180.1 microg/d) in the mountain community. The mean dietary selenium intake estimated from the SFFQ and average value of the normal portion size was 118.0 microg/d (n=123) (range 22.6-255.3 microg/d) in the coastal community. These estimated mean values exceeded the Japanese RDA, although the range of daily selenium intake was large. In the mountain community, fish made the largest contribution to dietary selenium intake (48.2% of daily total), followed by eggs (24.3%), and meat (17.0%). In the coastal community, fish accounted for 57.7% of daily total selenium intake, followed by meat (17.5%), and eggs (16.1%). In both districts, the total contribution of rice and wheat products was around 10%. It was found that the contribution of fish to dietary selenium intake was high and the contribution of cereals was low among Japanese.