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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 overview 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.

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 [micro]mol/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 [micro]mol/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.

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 RAR[beta]2 protein content dose-dependently compared with a casein diet, whereas supplemental ISF had no consistent effect. Neither RAR[beta] protein in the other tissues measured nor the other RAR (RAR[alpha] and RAR[gamma]) in the liver were affected by dietary SPI, indicating a tissue and isoform-specific effect of SPI. RAR[beta]2 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 RAR[beta] was significantly attenuated and the isoelectric points of RAR[beta]2 were shifted by dietary SPI. Overall, these results show for the first time, to our knowledge, that dietary soy proteins affect hepatic RAR[beta]2 protein content and RAR[beta] DNA binding activity, which may contribute to the suppression of retinoid-induced hypertriglyceridemia by SPI as reported.

Our previous studies showed that intake of 20% alcohol-washed soy protein isolate (SPI) significantly increased hepatic thyroid hormone receptor (TR) [beta]1 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 TR[beta]1 content and the binding of TR to thyroid hormone response element (I-RE) in rats. Sprague-Dawley rats (28 d old) were fed diets containing casein (20%) with or without isofiavone supplementation (50 mg/kg diet) or alcohol-washed SPI (5, 10, or 20%) for 90 d. The hepatic TR/31 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 TR/31 content in both male and female rats compared with a casein-based control diet. The increase in TR[beta]1 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 TR[beta]1 protein content and inhibits the binding of TR to target genes. Modulation of hepatic TR[beta]1, 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. J. Nutr. 135: 1631-1635, 2005. KEY WORDS: * rat * soy protein * isoflavones * thyroid hormone receptor * binding ability

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. TR[alpha]1, TR[alpha]2, and TR[beta]2 contents were not affected by SPI. However, the content of the 52-kDa TR[beta]1 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 TR[beta]1, whereas the high doses of isoflavones (250 and 1250 mg/kg diet) reduced the hepatic TR[alpha]1 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 TR[beta]1 expression, and that isoflavones reduce the hepatic TR[alpha]1 level in young male rats. The SPI-induced TR[beta]1 may play a role in mediating the hypocholesterolemic and lipid-lowering actions of soy protein. KEY WORDS: * rats * soy protein isolate * isoflavones * thyroid hormone receptors

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. KEY WORDS: * calcium * adequate intakes * tolerable upper intake levels * fortification

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. KEY WORDS: * copper status * copper chaperone * Cu/Zn superoxide dismutase * expression level * rats

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, 4.0 x = 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. J. Nutr. 132: 252-256, 2002. KEY WORDS: * dietary calcium * dietary phosphorus * nephrocalcinosis * female rats

The interaction of dietary selenium and iodine on the activities of the selenoenzymes, selenium-dependent glutathione peroxidase (GSH-Px), and type I deiodinase (DI-I), and the thyroid hormones thyroxine (T4) and triiodothyronine (T3) were studied. Male weanling Sprague-Dawley rats were fed an AIN-93G diet for 6 wk with modified selenium and iodine concentration as follows: three levels each of iodine and selenium (0.03, 0.2 added and 1.0 added mg iodine/kg diet, and 0.05, 0.18 added and 1.0 added mg selenium/kg diet) were used in a 3 x 3 factorial design. Renal, but not hepatic, DI-I activity was lower in rats with low selenium intake than in controls. Circulating T3 concentration was not affected by the dietary levels of iodine or selenium. Unlike in liver, kidney and erythrocytes, thyroidal GSH-Px activity was not lower than in controls in rats with low selenium intake, but was significantly higher when iodine intake was low. Significant interactions of iodine and selenium on serum T4 and thyroidal GSH-Px activity were observed. Serum T4 was maintained at control levels when both dietary iodine and selenium were low, but not when iodine alone, or selenium alone, was low. Activity of thyroidal GSH-Px was lowest in rats fed a diet containing high iodine and low selenium. The results suggest that high iodine intake, when selenium is deficient, may permit thyroid tissue damage as a result of low thyroidal GSH-Px activity during thyroid stimulation. A moderately low selenium intake normalized circulating T4 concentration in the presence of iodine deficiency. KEY WORDS: * iodine * selenium * selenoenzymes * thyroid hormones * rats

Previous studies have shown that canola oil (CA), compared with soybean oil (SO), shortens the life span of stroke-prone spontaneously hypertensive (SHRSP) rats, a widely used model for hemorrhagic stroke. SHRSP rats are highly sensitive to dietary cholesterol manipulations because a deficiency of membrane cholesterol makes their cell membranes weak and fragile. Phytosterols, abundant in CA but not in SO, can inhibit the absorption of cholesterol and also replace a part of cholesterol in cell membranes. This study was performed to determine whether the high concentration of phytosterols in CA might account for its life-shortening effect on SHRSP rats. Male, 35-d-old SHRSP rats (n = 28/group) were fed semipurified diets containing CA, SO, CA fortified with phytosterols (canola oil + phytosterols, CA + P), SO fortified with phytosterols (soybean oil + phytosterols, SO + P), corn oil (CO), olive oil (OO) or a fat blend that mimicked the fat composition of a representative Canadian diet (Canadian fat mimic, CFM; 10 g/100 g diet). These fats provided 97, 36, 207, 201, 114, 27 and 27 mg phytosterols/100 g diet, respectively. Ten rats from each group were killed after 30-32 d for blood and tissue analyses. The remaining rats (18/group) were used for determination of life span. The life span of SHRSP rats fed the high phytosterol oils (CA, CA + P, SO + P and CO) was significantly (P [is less than] 0.05) shorter than that of CFM- and SO-fed rats. At 30-32 d, the groups fed the high phytosterol oils had greater levels of phytosterols and significantly (P [is less than] 0.05) higher ratios of phytosterols/cholesterol in plasma, RBC, liver and kidney, and a significantly (P [is less than] 0.05) lower RBC membrane deformabilty index than the groups fed oils low in phytosterols (SO, OO and CFM). The mean survival times were correlated with RBC deformability index ([r.sup.2] = 0.91, P = 0.0033) and cholesterol concentration ([r.sup.2] = 0.94, P = 0.0016), and inversely correlated with RBC phytosterol concentration ([r.sup.2] = 0.58, P = 0.0798) and phytosterols/cholesterol ([r.sup.2] = 0.65, P = 0.0579), except in the OO group. This study suggests that the high concentration of phytosterols in CA and the addition of phytosterols to other fats make the cell membrane more rigid, which might be a factor contributing to the shortened life span of SHRSP rats. J. Nutr. 130: 1166-1178, 2000. KEY WORDS: * canola oil * cell membrane deformability * life span * phytosterols * stroke-prone spontaneously hypertensive rats

Tocopherols act as second-line defenses against increased stress of (n-3) fatty acids and should be considered in the study of protective enzymes responsible for the generation of reactive oxygen species. Furthermore, the higher urinary and thiobarbituric acid-reactive substances observed in female rats compared to male rats was explained on the basis of the difference among sexes in the pattern of fatty acid incorporation in tissues.