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Background: Adequate iodine intake is important for children and women of childbearing age because iodine is vital for fetal brain development and early life.Objective: Iodine status of children (n = 1875), adolescents (n = 557), and women of childbearing age (n = 567) was assessed using urinary iodine concentrations (UIC) from duplicate spot samples collected in the Canadian Health Measures Survey, cycle 5 (2016-2017).Methods: Daily iodine intakes were estimated from urinary iodine and creatinine concentrations using a formula based on iodine absorption and predicted 24-h creatinine excretion. Usual UIC and iodine intakes, adjusted for within-person variation, were estimated using the National Cancer Institute method. Iodine status was assessed by 1) comparing median UIC with WHO/UNICEF/ICCIDD reference ranges and 2) estimating the prevalence of inadequate and excessive intakes using the estimated average requirement (EAR) and tolerable upper intake level (UL) cut-point method, respectively.Results: Median UIC for males and females 6-11 or 12-19 y old were ≥100 μg/L, the lower cutoff for adequate intakes. For women 20-39 y old, the median UIC of an unadjusted sample was 81 μg/L (95% CI: 67, 95) and for the usual UIC was 108 μg/L (95% CI: 84, 131). The percentage of children 3 y old with iodine intake ≥EAR was 82% (95% CI: 75, 89). The corresponding estimates for males 4-8, 9-13, and 14-18 y old were 93% (95% CI: 88, 97), 91% (95% CI: 87, 96), and 84% (95% CI: 76, 91), respectively. Estimates for females 4-8, 9-13, 14-18, and 19-39 y old were 86% (95% CI: 83, 89), 87% (95% CI: 80, 95), 68% (95% CI: 55, 80), and 68% (95% CI: 59, 76), respectively. For all sex-age groups, 91-100% had iodine intakes ≤UL.Conclusions: Iodine intakes may be insufficient for some women of childbearing age. Public health policies and programs should continue to recommend that all women who could become pregnant, or women who are pregnant or breastfeeding, take a daily multivitamin-mineral supplement containing iodine. [ABSTRACT FROM AUTHOR]

The most commonly used indices for determining copper deficiency in humans are reduced serum/plasma copper concentration and decreased activity of ceruloplasmin and Cu/Zn superoxide dismutase (SOD1). However, these indicators are influenced by many factors unrelated to copper status and lack the sensitivity required to detect marginal deficiency, limiting their usefulness in many situations. In vivo, the insertion of copper into SOD1 is dependent on the copper chaperone for SOD1 (CCS). In this study, we explored the possibility that the expression level of CCS may reflect copper status and thus serve as a useful marker of copper nutriture. Weanling male Wistar rats were fed either a normal (5.3 mg Cu/kg diet), moderately deficient (0.84 mg Cu/kg diet) or deficient (0.34 mg Cu/kg diet) copper diet for 6 wk. Rats fed moderate and deficient diets showed differences (P < 0.05) in several hematological measurements, indicating varying degrees of copper deficiency in these groups. Copper-deficient rats had reduced (P < 0.05) liver and erythrocyte SOD1 activity and body weight. Western blot analysis revealed a dose-dependent increase (P < 0.05) in CCS expression in liver and erythrocytes of copper-deficient rats. We report CCS protein level as a novel marker for assessing copper status. [ABSTRACT FROM AUTHOR]

Nephrocalcinosis (NC) in female rats can complicate the interpretation of nutritional or toxicological studies involving the kidney. Recent reformulations of standardized rodent diets such as AIN-93G and NTP-2000 sought to optimize the dietary Ca:P ratio, an important etiologic factor in NC. The effect of increasing intakes of Ca and P together at their optimal molar ratio has not been systematically studied. Weanling female and male Sprague-Dawley rats were fed modified AIN-93G diets containing Ca and P at AIN-93G diet concentrations (5 g Ca + 3 g P/kg diet), with multiples of Ca and P at the same ratio (1.5x = 7.5 g Ca + 4.5 g P, 2.5x = 12.5 g Ca + 7.5 g P, 4.0x = 20.0 g Ca + 12.0 g P/kg diet), or Ca and P at concentrations found in the AIN-76A diet (5 g Ca + 5 g P/kg diet), for 16 wk. Incidence and severity of NC and kidney Ca concentration in female rats increased with dietary Ca and P, although not to levels in female rats fed at the AIN-76A Ca:P ratio. Male rats showed limited evidence of kidney Ca accumulation or NC. The concentrations of dietary Ca and P, as well as the ratio of these two elements, affected development of NC in female rats. [ABSTRACT FROM AUTHOR]

The Tolerable Upper Intake Levels (UL) for zinc for children were based on limited data and there is concern that the UL may be set too low. The first effect of excessive zinc intake is a reduction in copper status. The primary objective of this study was to examine the effect of zinc supplementation on copper status in children. Healthy, 6- to 8-y-old boys from Ontario, Canada were assigned to take a placebo (n = 10) or 5 mg (n = 10), 10 mg (n = 9), or 15 mg (n = 8) of zinc supplement daily for 4 me in a double-blinded, placebo-controlled, randomized trial. Biochemical measures were evaluated at baseline and after 2 and 4 mo of supplementation. Food records were completed near the baseline and 4-me visits. Age and anthropometric measurements did not differ (P> 0.05) between treatment groups at baseline. Mean zinc intakes from food alone (10.9-14.8 mg zinc/d) approached or exceeded the UL of 12 mg/d. Compared with the placebo group, the zinc groups had a greater change in the urine zinc: creatinine ratio at 4 mo (P = 0.02). Traditional (plasma copper and ceruloplasmin activity) and more sensitive biomarkers of copper status, including erythrocyte SOD1 activity and the erythrocyte CCS:SOD1 protein ratio, were unchanged in zinc-supplemented boys, demonstrating that copper status was not depressed. Serum lipid measures and hemoglobin concentrations were also unaffected and gastrointestinal symptoms were not reported. These data provide evidence in support of the need for reexamining the current UL for zinc for children. [ABSTRACT FROM AUTHOR]

Interest in the health effects of foods by both industry and consumers has put a spotlight on the role of health claims on foods in Canada. The current regulatory framework governing the use of different health claims on foods in Canada is described and compared with international approaches. Similarities were observed in how risk-reduction claims for serious diseases are managed in the United States, European Union and proposed by Food Standards Australia New Zealand, including the need for premarket authorization and the requirement for a high level of certainty based on the totality of evidence in substantiating this type of claim. However, approaches to permitting function claims other than those for the well-established functions of known nutrients are divergent among the jurisdictions compared. Canada also differs from other jurisdictions in not establishing core nutritional criteria for foods carrying disease risk-reduction claims. A brief over- view of the status in Canada of a number of disease risk-reduction claims that have been approved in the United States, based on significant scientific agreement under the Nutrition Labeling and Education Act or through authoritative statements under the Food and Drug Administration Modernization Act, is also provided. [ABSTRACT FROM AUTHOR]

ATPase/ATP synthase plays important roles in the regulation of carbohydrate, protein, and lipid metabolism through modulating energy homeostasis. The purpose of this study was to examine the effects of feeding soy proteins and isoflavones (ISF) on the enzymatic activity and protein modification of hepatic mitochondrial ATPase/ATP synthase. In Expt. 1, Sprague-Dawley rats aged 50 d were fed diets containing either 20% casein or 20% alcohol-washed soy protein isolate (SPI) with or without supplemental ISF (770.7 micromol/kg diet) for 70 d. In Expt. 2, weanling Sprague-Dawley rats were fed diets containing 20% casein with or without added ISF (154.1 micromol/kg diet) or 20% SPI for 90 d. Hepatic mitochondrial ATPase activity was significantly higher in the rats fed SPI than in those fed casein. Addition of ISF to SPI eliminated the action of SPI. ATPase/ATP synthase beta protein contents in the liver were unchanged; however, its patterns measured by 2-dimensional Western blot were different among dietary groups. The rats fed SPI or SPI plus ISF had 3 more major protein spots with the same molecular weights (80 kDa and 55 kDa) as those presented in the rats fed casein but with different isoelectric points. Pretreatment of hepatic mitochondrial proteins from the rats fed casein with alkaline phosphatase produced the same ATPase/ATP synthase beta patterns as observed in the SPI-fed rats and significantly elevated the ATPase activity. These results suggest that consumption of soy proteins increases hepatic ATPase activity, which might be a consequence of increased dephosphorylation or decreased phosphorylation of the mitochondrial ATPase/ATP synthase beta protein. [ABSTRACT FROM AUTHOR]

ATPase/ATP synthase plays important roles in the regulation of carbohydrate, protein, and lipid metabolism through modulating energy homeostasis. The purpose of this study was to examine the effects of feeding soy proteins and isoflavones (ISF) on the enzymatic activity and protein modification of hepatic mitochondrial ATPase/ATP synthase. In Expt. 1 Sprague-Dawley rats aged 50 d were fed diets containing either 20% casein or 20% alcohol-washed soy protein isolate (SPI) with or without supplemental ISF (770.7 µmol/kg diet) for 70 d. In Expt. 2, weanling Sprague-Dawley rats were fed diets containing 20% casein with or without added ISF (154.1 µmol/kg diet) or 20% SPI for 90 d. Hepatic mitochondrial ATPase activity was significantly higher in the rats fed SPI than in those fed casein. Addition of ISF to SPI eliminated the action of SPI. ATPase/ATP synthase β protein contents in the liver were unchanged; however, its patterns measured by 2-dimensional Western blot were different among dietary groups. The rats fed SPI or SPI plus ISF had 3 more major protein spots with the same molecular weights (80 kDa and 55 kDa) as those presented in the rats fed casein but with different isoelectric points. Pretreatment of hepatic mitochondrial proteins from the rats fed casein with alkaline phosphatase produced the same ATPase/ATP synthase β patterns as observed in the SPI-fed rats and significantly elevated the ATPase activity. These results suggest that consumption of soy proteins increases hepatic ATPase activity, which might be a consequence of increased dephosphorylation or decreased phosphorylation of the mitochondrial ATPase/ATP synthase β protein. [ABSTRACT FROM AUTHOR]

Retinoic acid receptors (RAR) belong to the same nuclear receptor superfamily as thyroid hormone receptors (TR) that were previously shown to be modulated by dietary soy protein isolate (SPI). This study has examined the effect of dietary SPI and isoflavones (ISF) on hepatic RAR gene expression and DNA binding activity. In Expt. 1, Sprague-Dawley rats were fed diets containing 20% casein or 20% alcohol-washed SPI in the absence or presence of increasing amounts of ISF (5-1250 mg/kg diet) for 70, 190, or 310 d. In Expt. 2, weanling Sprague-Dawley rats were fed diets containing 20% casein with or without supplemental ISF (50 mg/kg diet) or increasing amounts of alcohol-washed SPI (5, 10, and 20%) for 90 d. Intake of soy proteins significantly elevated hepatic RARbeta2 protein content dose-dependently compared with a casein diet, whereas supplemental ISF had no consistent effect. Neither RARbeta protein in the other tissues measured nor the other RAR (RARalpha and RARgamma) in the liver were affected by dietary SPI, indicating a tissue and isoform-specific effect of SPI. RARbeta2 mRNA abundances were not different between dietary groups except that its expression was markedly suppressed in male rats fed SPI for 310 d. DNA binding activity of nuclear RARbeta was significantly attenuated and the isoelectric points of RARbeta2 were shifted by dietary SPI. Overall, these results show for the first time, to our knowledge, that dietary soy proteins affect hepatic RARbeta2 protein content and RARbeta DNA binding activity, which may contribute to the suppression of retinoid-induced hypertriglyceridemia by SPI as reported. [ABSTRACT FROM AUTHOR]

Retinoic acid receptors (RAR) belong to the same nuclear receptor superfamily as thyroid hormone receptors (TR) that were previously shown to be modulated by dietary soy protein isolate (SPI). This study has examined the effect of dietary SPI and isoflavones (ISF) on hepatic RAR gene expression and DNA binding activity. In Expt. 1 Sprague-Dawley rats were fed diets containing 20% casein or 20% alcohol-washed SPI in the absence or presence of increasing amounts of 1SF (5-1250 mg/kg diet) for 70, 190, or 310 d. In Expt. 2, weanhing Sprague-Dawley rats were fed diets containing 20% casein with or without supplemental 1SF (50 mg/kg diet) or increasing amounts of alcohol-washed SPI (5, 10, and 20%) for 90d. Intake of soy proteins significantly elevated hepatic RARβ2 protein content dose-dependently compared with a casein diet, whereas supplemental 1SF had no consistent effect. Neither RARβ protein in the other tissues measured nor the other RAR IRARα and RARγ) in the liver were affected by dietary SPI, indicating a tissue and isoform-specific effect of SPI. RARβ2 mRNA abundances were not different between dietary groups except that its expression was markedly suppressed in male rats fed SPI for 310 d. DNA binding activity of nuclear RARβ was significantly attenuated and the isoelectric points of RARβ2 were shifted by dietary SPI. Overall, these results show for the first time, to our knowledge. that dietary soy proteins affect hepatic RARβ2 protein content and RARβ DNA binding activity, which may contribute to the suppression of retinoid-induced hypertriglyceridemia by SPI as reported. [ABSTRACT FROM AUTHOR]

Fortification with calcium to increase dietary intakes of this mineral is currently under evaluation in Canada. To model the potential dietary consequences of food fortification, data from a large national survey of Canadians (n = 1543) were used. Food fortification scenarios were based on reference amounts for labeling requirements. Consumption of milk, cheese and other dairy products was associated with high calcium intakes, and there was a low prevalence of inadequacy in men < 50 y old; however, other age-sex groups had lower intakes. The aim of the fortification modeling was to determine which scenario would most effectively reduce the proportion of the population with low intakes of calcium while minimizing the proportion of individuals who exceeded the tolerable upper intake level (UL). Given the correlation between energy and calcium (r = 0.60, P < 0.01), it appeared that any fortification scenario sufficient to increase the mean intake for women to near the adequate intake led to 6-7% of the men having calcium intakes above the UL. The results suggest that fortification of widely consumed foods is not a realistic way to address the issue of low calcium intakes and illustrate the need for concern about the growing use of fortification practices. [ABSTRACT FROM AUTHOR]

Our previous studies showed that intake of 20% alcohol-washed soy protein isolate (SPI) significantly increased hepatic thyroid hormone receptor (TR) beta1 protein content in rats. However, whether SPI influences the binding ability of TR to its target genes is unknown. The purpose of this study was to examine the effect of increasing amounts of dietary SPI on hepatic TRbeta1 content and the binding of TR to thyroid hormone response element (TRE) in rats. Sprague-Dawley rats (28 d old) were fed diets containing casein (20%) with or without isoflavone supplementation (50 mg/kg diet) or alcohol-washed SPI (5, 10, or 20%) for 90 d. The hepatic TRbeta1 protein content was measured by Western blot, and the binding ability of TR to DNA was examined by electrophoretic mobility shift assay. Consumption of the 20% SPI diet increased pancreatic relative weight and decreased spleen relative weight. Intake of SPI markedly elevated TRbeta1 content in both male and female rats compared with a casein-based control diet. The increase in TRbeta1 in females was much higher than that in males. Interestingly, the binding abilities of TR to DNA were significantly inhibited by increasing amounts of dietary SPI in female rats. In conclusion, this study shows for the first time that dietary SPI increases hepatic TRbeta1 protein content and inhibits the binding of TR to target genes. Modulation of hepatic TRbeta1, a key regulator of gene expression involved in lipid metabolism, by SPI may be a novel mechanism by which soy components lower blood lipid level and exert their hypocholesterolemic actions.

Thyroid hormone receptors (TRs) are regulators of many genes involved in cholesterol and lipid metabolism. The purpose of this study was to examine the effect of soy protein isolate (SPI) and isoflavones on hepatic TRs in rats. In Expt. 1, Sprague-Dawley rats were fed diets containing either casein or alcohol-washed SPI with or without isoflavone supplementation (5-1250 mg/kg diet) for 70, 190, and 310 d. The offspring (F1) were fed the same diets as their parents (F0). In Expt. 2, Sprague-Dawley rats were fed diets containing casein or casein plus isoflavones (50-400 mg/kg diet) for 120 d. The mRNA and protein contents of the hepatic TRs were measured by semiquantitative RT-PCR and Western blot, respectively. TRalpha1, TRalpha2, and TRbeta2 contents were not affected by SPI. However, the content of the 52-kDa TRbeta1 protein, the major isoform present in the liver, was markedly increased by dietary SPI in both sexes of F0 and F1 compared with casein. The supplemental isoflavones had no effect on TRbeta1, whereas the high doses of isoflavones (250 and 1250 mg/kg diet) reduced the hepatic TRalpha1 protein content in F1 male rats on d 28. SPI had no effect on total T3 and T4 levels. However, higher dose of supplemental isoflavones markedly increased T4 level in female rats. Overall, this study demonstrates for the first time that SPI upregulates hepatic TRbeta1 expression, and that isoflavones reduce the hepatic TRalpha1 level in young male rats. The SPI-induced TRbeta1 may play a role in mediating the hypocholesterolemic and lipid-lowering actions of soy protein.