Search

Non-nutritive sweeteners are thought to be useful replacements for caloric sweeteners in sweet food and beverages, since the reduction in energy and carbohydrate intake may lead to health benefits stemming from weight management and glycemic control. However, the potential effects of non-nutritive sweeteners on glucose metabolism and gut hormones have not been determined definitively. Here, the available evidence of the effects of aspartame and sucralose consumption on glucose metabolism and gut hormones is reviewed. A majority of studies have found that consumption of aspartame or sucralose has no effect on concentrations of blood glucose, insulin, or gut hormones; however, 2 trials have shown that aspartame consumption affects glucose, insulin, and glucagon-like peptide 1 concentrations, while only a few trials have shown that sucralose consumption affects glucose, insulin, and glucagon-like peptide 1 concentrations. One study found higher glucose concentrations after sucralose consumption, while 3 studies found lower concentrations and 33 studies found no change in glucose concentrations. Moreover, only 4 studies reported increased concentrations of glucagon-like peptide 1. Three studies reported decreased insulin sensitivity following sucralose consumption, while 1 trial reported an increase in insulin sensitivity. In summary, the evidence from the clinical trials conducted to date is contradictory because of the different protocols used. [ABSTRACT FROM AUTHOR]

This study aimed to determine the effect of pure forms of sucralose and aspartame, in doses reflective of commonconsumption, on glucose metabolism. Healthy participants consumed pure forms of a non-nutritive sweetener (NNS) that weremixed with water and standardized to doses of 14% (0.425 g) of the acceptable daily intake (ADI) for aspartame and 20% (0.136 g)of the ADI for sucralose every day for 2 weeks. Blood samples were collected and analyzed for glucose, insulin, active glucagonlikepeptide-1 (GLP-1), and leptin. Seventeen participants (10 females and 7 males; age, 24 �} 6.8 years; body mass index, 22.9 �}2.5 kg/m2) participated in the study. The total area under the curve values of glucose, insulin, active GLP-1 and leptin were similarfor the aspartame and sucralose treatment groups compared with the baseline values in healthy participants. There was nochange in insulin sensitivity after NNS treatment compared with the baseline values. These findings suggest that daily repeatedconsumption of pure sucralose or aspartame for 2 weeks had no effect on glucose metabolism among normoglycaemic adults.However, these results need to be tested in studies with longer durations. [ABSTRACT FROM AUTHOR]

Background: Iron is an essential nutrient for normal growth and neurodevelopment of infants. Iron deficiency (ID) remains the most common micronutrient deficiency worldwide. There are convincing data that ID is associated with negative effects on neurological and psychomotor development. Objectives: In this review, we provide an overview of current knowledge of the importance of iron in normal term breast-fed infants with a focus on recommendations, metabolism, and iron requirements. Conclusions: Health organizations around the world recommend the introduction of iron-rich foods or iron supplements for growing infants to prevent ID. However, there is no routine screening for ID in infancy. Multicenter trials with long-term follow-up are needed to investigate the association between iron fortification/supplementation and various health outcomes. [ABSTRACT FROM AUTHOR]

Abstract: Dietary energy restriction (ER) offers certain health benefits, particularly when ER is controlled through manipulation of dietary fats. Our hypothesis is that cellular immunity is modulated by dietary ER. Furthermore, we believe that the immune response may differ between spleen and colon because their lymphatic and vascular organization is different. The objective of the study was to test this hypothesis by determining the effects of dietary ER through manipulation of energy intake from high-fat (HF) diets on the expression and frequency of the CD4+ (T-helper/T-inducer) and CD8+ (T-cytotoxic/T-suppressor) cells, CD45RA (B-cell–specific marker), and immunoglobulins (Ig) A-, G-, and M-bearing cells in spleen and colon in rats by immunohistochemical method. Rats fed the HF diet had a significantly (P < .05) reduced number of immune cells as compared with those fed ER diets. Energy-restricted diet–fed rats showed higher (P < .05) numbers of CD4+, CD8+, IgA, IgM, IgG, and CD45RA cells in spleen and CD4+, IgA, and CD45RA cells in colonic lamina propria. The IgA-containing cells were markedly higher in the colon compared with the spleen. No change occurred in the number of IgM- and IgG-containing cells in colonic tissues between groups, except for the 20% ER group where IgM-labeled cells were higher (P < .05) compared with HF and 40% ER groups. These findings suggest that ER may modulate adaptive immune function and that CD4+ and IgA cells may serve as biological indicators for dietary energy-modulated immunoresponse in spleen and colon, respectively. [Copyright &y& Elsevier]

Lower body fat percentage is positively associated with climbing performance. This may lead climbers to practice unhealthy diet restriction when no sport-specific nutrition information exists. This study examined whether prolonged diet restriction affects body composition, oxidative stress, or other potential health risks in outdoor rock climbers. Two healthy male climbers conducted a 5 week rock climbing trip with a limited food budget ($1 each per day). Subjects underwent an energy restriction of approximately 40%. Loss of body weight and fat mass at week 5 were 5.8% and 16.1%, respectively, and were accompanied by significant subcutaneous fat loss in the iliac crest and abdomen. Triacylglycerols (TG), free fatty acids and C-reactive protein (CRP) dramatically decreased from baseline to week 2, and then maintained the lower level until week 5. Plasma vitamin C was below the normal range, and F2-isoprostanes, a marker of oxidative stress, continuously increased to week 5. Superoxide dismutase and glutathione peroxidase increased to week 2, but had returned to baseline levels at week 5. These results indicate that prolonged reduced energy intake while climbing may have an impact on weight loss and fat mass loss, which may contribute to low circulating TG and CRP, indicating improvements in markers of cardiovascular risk, and may lead to increased oxidative stress and reduced circulating antioxidants. Further studies are warranted to determine whether antioxidant supplementation or increased energy intake reduce oxidative stress. [ABSTRACT FROM AUTHOR]

Abstract: Stress due to reactive oxygen species (ROS) may lead to neonatal diseases, such as necrotizing enterocolitis and respiratory distress. Enteral supplements for premature infants (PREM) added to human milk (HM) to increase nutrient content may induce lipid oxidation due to free radical formation via Fenton chemistry. We hypothesized that ferrous iron and vitamin C-containing supplements added to HM in vitro cause oxidation of milk fats, affect intracellular redox balance, and induce DNA damage. Lipid peroxidation in HM was measured by FOX-2 and TBARS assays; fatty acid composition of supplemented HM was measured by gas chromatography. Two cell culture bioassays were used for assessing either intracellular oxidative stress or DNA damage: the former involved Caco-2BBe cells, a secondary differentiated cell line, and the latter utilized FHS-74 Int cells, a primary fetal small intestinal culture. Lipid oxidation products of HM increased after the addition of iron alone, iron and vitamin C, or iron and a vitamin C-containing supplement (Trivisol, TVS). A reduced content of mono and polyunsaturated fatty acids in HM was also observed. Iron, not iron+vitamin C, but iron+TVS induced significant intracellular oxidative stress in FHS-74 Int cells. In contrast, iron, either alone or in combination with TVS or vitamin C, increased DNA damage in Caco-2BBE cells. Iron supplementation may increase oxidative stress in PREM infants and should be given separately from vitamin C-containing supplements. [Copyright &y& Elsevier]

Abstract: Neural tube defects are congenital abnormalities caused by failure of the neural tube to close during embryogenesis. We investigated trace elements (zinc, copper, manganese, cobalt, nickel, molybdenum, cadmium), livers, pancreata, sciatic nerves, diaphragms, and kidneys collected at autopsy from 33 anencephalic fetuses and 22 control fetuses. Collections were done on the right side using a titanium scalpel, plastic forceps, and acid-washed materials. Samples were wet ashed and analyzed using inductively coupled plasma mass spectrometry. The gestational age and birth weight (mean ± SD) of anencephalic fetuses were 25.8 ± 8 weeks and 729 ± 879 g, respectively; those of control fetuses, 28 ± 8 weeks and 1340 ± 1216 g, respectively. Liver concentrations (ppm, dry weight, mean ± SEM) of Zn (1075 ± 56 vs 668 ± 75; P = .001) increased in anencephalic fetuses, suggesting defective transport of Zn. Whether this is part of the cause of neural tube defects or a result of the disease is unclear. [Copyright &y& Elsevier]

Premature infants are vulnerable to tissue damage due to supplemental oxygen intake. We hypothesized that oxidative injury as indicated by plasma malondialdehyde (MDA) would be related to nutrient intakes, RBC superoxide dismutase and catalase, plasma vitamin E, and mean daily oxygen exposure (FiO2). Therefore 43 infants < 1500 g birthweight were examined 3 times during the first 28 days of life. Whole blood was collected at Days 4, 14, 28. On Day 4, MDA was correlated with FiO2 (r = +0.40, p = 0.001) and inversely correlated with plasma vitamin E (r = -0.35, p = 0.028). Plasma vitamin E levels were correlated with vitamin E intakes on Day 4 (r = +0.25, p = 0.02).Plasma data indicated that not all infants handled vitamin E intakes the same. Catalase was correlated with FiO2 at Day 4 (r = +0.34, p = 0.037), suggesting up regulation of antioxidant defences with early oxygen exposure. Early nutrient intervention may decrease tissue damage from oxygen exposure. [Copyright &y& Elsevier]

A letter to the editor is presented that reports the results of a study on the nutritional factors affecting risk for heart disease in firefighters.

Presents a letter to the editor regarding a study that determined whether folic acid reduces homocysteine levels and masks vitamin B-12 deficiency in elderly people.

Chemical screening of digested human milk protein using the oxygen radical absorbance capacity (ORACFL) antioxidant assay confirmed the presence of a peptide fraction (PF23) with high antioxidant activity [5.53 mmol Trolox equivalents (TE)/g] that contained tryptophan as a main component. We evaluated the effects of both PF23 and tryptophan alone on the modulation of oxidative stress in cultured intestinal cells using a dichlorofluorescein diacetate probe. Despite the high ORACFL value, PF23 enhanced (P< 0.05)2, 2′-azobis (2-amidinopropane) dihydrochloride (peroxyl radical generator)-induced intracellular oxidation in the Caco-2 human adenocarcinoma cell line, suggesting prooxidant activity. Compared to selected peptide fractions with relatively lower ORACFL values, PF23 induced oxidative stress more than all other peptide fractions tested (P < 0.05) and contained more tryptophan than the others (P < 0.05). Similar prooxidant activity was observed for tryptophan when it was added to culture medium for both the Caco-2 cells and FHs 74 Int primary fetal enterocytes, while also exhibiting a high ORACFL value (9.69 mmol TE/g). The effect of tryptophan that involves activation of the Nrf-2 pathway and transcription of antioxidant enzymes was therefore investigated in FHs 74 Int cells. Exposure of infant intestinal cells to tryptophan resulted in Nrf-2 activation and an increase in the gene transcript level of glutathione peroxidase 2. We conclude that tryptophan-induced oxidative stress associated with tryptophan-containing milk peptides induces an adaptive response that involves the activation of the antioxidant responsive signaling pathway in intestinal cells. [ABSTRACT FROM AUTHOR]

The up to 60% of non-absorbed dietary iron can participate in the generation of ROS in the colon. Measuring ROS production in fecal matter can be difficult and tedious. Our purpose was to measure the effect of supplemental iron on ROS production in human feces. Four healthy male subjects received 120 mg of iron as ferrous sulfate during 2 periods of 7 consecutive days; in the second period, 5 ml of refined palm oil were added to the iron dose. Stool samples were collected at baseline, during supplementation days, and 11 days later. They were analyzed using a calibrated HPLC method proposed by Owen, et al, 2000, validated by a hypoxanthine/xanthine oxidase model. ROS production (expressed as mg of hydroxylated products resulting from the free-radical attack on salicylic acid) showed a mean increase from 0.26 mg at baseline to 0.33 mg during supplementation and decreased to 0.27 mg after iron supplementation alone. With 5 ml of palm oil added to the iron dose, the response increased on average, from 0.27 mg at baseline to 0.35 mg during supplementation and decreased to 0.27 mg after supplementation. We concluded that the in vitro assay can be used in a human metabolic study context. [ABSTRACT FROM AUTHOR]

Abstract: Human milk pepsin and pancreatin digests were separated using molecular membrane and reverse phase chromatography. Chemical screening of the resulting fractions using the ORAC antioxidant assay yielded a peptide fraction (PF-23) with high antioxidant activity (5207μM Trolox Equivalents (TE)/g). Tandem mass spectrometry allowed the identification of twenty peptides. Eight small molecular weight peptides from 4 to 6 amino acids were synthesised and screened for antioxidant properties using ORAC and linoleic acid emulsion. On ORAC, the peptides YGYTGA (5169μM TE/mmol) and ISELGW (4479μM TE/mmol) were the most active. At 250μM peptide ISELGW and its derivatives significantly reduced hydroperoxides formed during autoxidation of linoleic acid for 4days at 50°C. Further testing of these peptides may allow their inclusion in infant formulas to reduce the incidence of oxidative stress-mediated diseases in newborns. [ABSTRACT FROM AUTHOR]

Prophylactic doses of 120mg of iron (Fe) are commonly used to prevent Fe-deficiency anemia in vulnerable populations, especially in developing countries. Evidence shows that residual Fe in the large bowel may alter the normal antioxidant capacity of the fecal stream. Our objective was to evaluate the effect of dietary antioxidants from the Carotino Tocotrienol-Carotene Mixed Concentrate (CTCMC) on the depletion of fecal antioxidant capacity by oral Fe supplementation. In total, 17 healthy male adults participated in the 2 phases of the study, 5 in the pilot study and 12 in the definitive intervention trial. Participants received different treatments, separated by washout periods. These included: 120 mg Fe; 120 mg Fe and refined palm oil (FeOiI); and 120 mg Fe in refined palm oil combined with 1 of 2 dosages (0.4 g and 0.8 g) of CTCMC/5 mL of refined palm oil (CTCB and CTCA treatments, respectively). Fecal samples were collected and analyzed to quantify the products of hydroxyl radical attack on salicylic acid (2,5 dihydroxybenzoic acid, 2,3-dihydrobenzoic acid, and catechol) at baseline and after active supplementation. Fe supplementation in either form (Fe or FeOil treatments) increased the concentrations of hydroxylated compounds in fecal samples. The production of hydroxylated compounds was significantly lower in treatments CTCB and CTCA than in the FeOil reference. Baseline antioxidant capacity state was virtually restored with dietary carotenoids and tocotrienols from the CTCMC. In conclusion, dietary antioxidants can reverse the depletion of fecal antioxidant capacity induced by oral Fe supplements. [ABSTRACT FROM AUTHOR]

Abstract: The oxygen radical absorbance capacity (ORAC–FL) assay, a useful measure of the antioxidant capacity (AC) reported for some biological samples, supplements, and food samples, was standardized and validated for measuring AC of human milk. Limits of linearity, precision and accuracy of the ORAC–FL assay were made by constructing a Trolox Calibrator which included the addition of human milk as the sample matrix. AC assay results indicated excellent linearity (R 2 =0.990±0.005), precision (2.2%) and accuracy on recovery (94.8±3.2%) over a wide range of Trolox concentrations. To validate the assay further, mature milk samples were collected from 100 lactating mothers in Vancouver and Winnipeg, and were measured for vitamin E isomers by HPLC and AC using the standardized ORAC–FL assay. Alpha-tocopherol (α-Toc) was the major vitamin E isomer detected in human milk, established using both ultra-violet and fluorescent detection methods. Milk α-Toc concentrations were found to correlate significantly (P <0.01) with ORAC–FL assay values in milk obtained from mothers in both Vancouver (R =0.439, n =60) and Winnipeg (R =0.408, n =40). Although milk is a complex matrix with multiple components possessing potential antioxidant activity, our results indicated that the ORAC–FL assay is a very useful indicator for assessing the antioxidant capacity of human milk. [Copyright &y& Elsevier]

Abstract: Objective: It is important to understand the difference and similarity in antioxidant capacity and aroma quality between formula and breast milk for purposes of modifying infant formulas. We evaluated the antioxidant properties and aroma quality of infant formula and breast milk. Methods: Six breast milk samples and four infant formulas were used. Antioxidant properties were measured using the following methods: 2,2-diphenyl-1-picryhydrazyl free radical scavenging capacity, oxygen radical absorbance capacity, total phenolic content, and phenolic composition. Aroma quality was determined using the electronic nose. Results: The 2,2-diphenyl-1-picryhydrazyl free radical scavenging activity for formula and breast milk ranged from 45.3% to 61.8% and from 52.8% to 61.2%, respectively. Oxygen radical absorbance capacity ranged from 28.8 to 31.9 g/kg for formula and from 25.5 to 39.2 g/kg for breast milk. Total phenolic content ranged from 422 to 751 mg/kg and from 329to 797 mg/kg for formula and milk, respectively. p-Hydroxybenzoic acid, p-coumaric acid, and ferulic acid were detected with values ranging from 614 to 635, 1391 to 1444, and 1425 to 1490 μg/kg in breast milk and from 783 to 3594, 1449 to 1510, and 1447 to 1561 μg/kg in formulas. Electronic nose results indicated that the aroma quality of formula controls 2, 3, and 4 was similar to that of breast milk. Conclusion: Differences and similarities in antioxidant properties and aroma quality were found among some of the formulas and breast milk. The contribution of phenolic acids to total antioxidant capacity was limited. [Copyright &y& Elsevier]

We utilized a vitamin D receptor (VDR) gene knockout model to study the effects of maternal and fetal absence of VDR on maternal fertility, fetal-placental calcium transfer, and fetal mineral homoeostasis. Vdr null mice were profoundly hypocalcemic, conceived infrequently, and had significantly fewer viable fetuses in utero that were also of lower body weight. Supplementation of a calcium-enriched diet increased the rate of conception in Vdr nulls but did not normalize the number or weight of viable fetuses. Among offspring of heterozygous (Vdr+/-) mothers (wild type, Vdr+/-, and Vdr null fetuses), there was no alteration in serum Ca, P, or Mg, parathyroid hormone, placental 45Ca transfer, Ca and Mg content of the fetal skeleton, and morphology and gene expression in the fetal growth plates. Vdr null fetuses did have threefold increased 1,25-dihydroxyvitamin D levels accompanied by increased 1α-hydroxylase mRNA in kidney but not placenta; a small increase was also noted in placental expression of parathyroid hormone-related protein (PTHrP). Among offspring of Vdr null mothers, Vdr+/- and Vdr null fetuses had normal ionized calcium levels and a skeletal ash weight that was appropriate to the lower body weight. Thus our findings indicate that VDR is not required by fetal mice to regulate placental calcium transfer, circulating mineral levels, and skeletal mineralization. Absence of maternal VDR has global effects on fetal growth that were partly dependent on maternal calcium intake, but absence of maternal VDR did not specifically affect fetal mineral homeostasis. [ABSTRACT FROM AUTHOR]

We used the calcitonin/calcitonin gene-related peptide (CGRP)-α gene knockout model (Ct/Cgrp null) to determine whether calcitonin and CGRPα are required for normal fetal mineral homeostasis and placental calcium transfer. Heterozygous (Ct/Cgrp+/-) and Ct/Cgrp null females were mated to Ct/Cgrp+/- males. One or two days before term, blood was collected from mothers and fetuses and analyzed for ionized Ca, Mg, P, parathyroid hormone (PTH), and calcitonin. Amniotic fluid was collected for Ca, Mg, and P. To quantify skeletal mineral content, fetuses were reduced to ash, dissolved in nitric acid, and analyzed by atomic absorption spectroscopy for total Ca and Mg. Placental transfer of 45Ca at 5 min was assessed. Ct/Cgrp null mothers had significantly fewer viable fetuses in utero compared with Ct/Cgrp+/- and wild type mothers. Fetal serum Ca, P, and PTH did not differ by genotype, but serum Mg was significantly reduced in null fetuses. Placental transfer of 45Ca at 5 min was normal. The calcium content of the fetal skeleton was normal; however, total Mg content was reduced in Ct/Cgrp null skeletons obtained from Ct/Cgrp null mothers. In summary, maternal absence of calcitonin and CGRPα reduced the number of viable fetuses. Fetal absence of calcitonin and CGRPα selectively reduced serum and skeletal magnesium content but did not alter ionized calcium, placental calcium transfer, and skeletal calcium content. These findings indicate that calcitonin and CGRPα are not needed for normal fetal calcium metabolism but may regulate aspects of fetal Mg metabolism. [ABSTRACT FROM AUTHOR]

AbstractBackground: Newfoundland has one of the highest rates of neural tube defects in North America. Given the association between low maternal folic acid levels and neural tube defects, a cross-sectional study was conducted to obtain baseline data on the folate and vitamin B[sub 12] status of a sample of women in Newfoundland who were pregnant.Methods: Blood samples were collected between August 1996 and July 1997 from 1424 pregnant women in Newfoundland during the first prenatal visit (at approximately 16 weeks' gestation); this represented approximately 25% of the women in Newfoundland who were pregnant during this period. The samples were analysed for serum folate, vitamin B[sub 12], red blood cell folate and homocysteine.Results: Median values for serum folate, red blood cell folate and serum vitamin B[sub 12] were 25 nmol/L, 650 nmol/L and 180 pmol/L, respectively. On the basis of the interpretive criteria used for red blood cell folate status, 157 (11.0%) of the 1424 women were deficient (< 340 nmol/L) and a further 180 (12.6%) were classified as indeterminate (340-420 nmol/L). Serum homocysteine levels, measured in subsets of the red blood cell folate status groups, supported the inadequate folate status. Serum vitamin B[sub 12] levels of 621 (43.6%) women were classified as deficient or marginal; however, the validity of the interpretive criteria for pregnant women is questionable.Interpretation: A large proportion of pregnant women surveyed in Newfoundland in 1997 had low red blood cell folate levels. [ABSTRACT FROM AUTHOR]

Over a period of 9 wks, in 8 healthy Guatemalan male volunteers, we serially measured serum levels of interleukin-4 (IL-4) and tumor necrosis factor (TNF-α) (markers of inflammation) and urinary excretion of thiobarbituric acid reactive substances (TBARS), isoprostanes (ISO), and 8OH-deoxy-guanosine at baseline and 1, 2, and 7 days after oral doses of iron: 0, 15, 30, 60, 120 and 240 mg given as single doses at 1-wk (0-60 mg) or 2-wk (120, 240 mg) intervals In most instances, serum IL-4 was below the detection limit. Intraindividual CVs for baseline TNF-α ranged from 13.6-46.7% (mean, 24.1%) over 6 samplings. For 6 consecutive urinary measures, the baseline within-individual CVs ranged from 23.4-74.9% (mean, 37.3%) for TBARS, 13.4-149.7% (mean, 63.2%) for ISO, and 35.2-77.3% (mean, 49.7%) for 8OhdG. With respect to within-group stability, increasing iron dosage had no consistent effect on the variance of any of the 2 circulating inflammatory or 3 urinary oxidation biomarkers. These intra- and inter-subject variation analyses inform the estimation of critical sample-size for the design of prospective intervention trials using the respective modern biomarkers as outcome variables. [ABSTRACT FROM AUTHOR]