Moderate wine consumption has been shown to lower cardiovascular risk. One of the mechanisms could involve the control of postprandial hyperlipaemia, a well-defined risk factor for atherosclerosis, reasonably by reducing the absorption of lipid oxidised species from the meal. The objective of the present study was to investigate whether wine consumption with the meal is able to reduce the postprandial increase in plasma lipid hydroperoxides and cholesterol oxidation products, in human subjects. In two different study sessions, twelve healthy volunteers consumed the same test meal rich in oxidised and oxidisable lipids (a double cheeseburger), with 300 ml of water (control) or with 300 ml of red wine (wine). The postprandial plasma concentration of cholesterol oxidation products was measured by GC–MS. The control meal induced a significant increase in the plasma concentration of lipid hydroperoxides and of two cholesterol oxidation products, 7-β-hydroxycholesterol and 7-ketocholesterol. The postprandial increase in lipid hydroperoxides and cholesterol oxidation products was fully prevented by wine when consumed with the meal. In conclusion, the present study provides evidence that consumption of wine with the meal could prevent the postprandial increase in plasma cholesterol oxidation products.

Although dietary nutrient intake is often adequate, nutritional supplement use is common among elite athletes. However, high-dose supplements or the use of multiple supplements may exceed the recommended daily allowance (RDA) of particular nutrients or even result in a daily intake above tolerable upper limits (UL). The present case report presents nutritional intake data and supplement use of a highly trained male swimmer competing at international level. Habitual energy and micronutrient intake were analysed by 3 d dietary reports. Supplement use and dosage were assessed, and total amount of nutrient supply was calculated. Micronutrient intake was evaluated based on RDA and UL as presented by the European Scientific Committee on Food, and maximum permitted levels in supplements (MPL) are given. The athlete's diet provided adequate micronutrient content well above RDA except for vitamin D. Simultaneous use of ten different supplements was reported, resulting in excess intake above tolerable UL for folate, vitamin E and Zn. Additionally, daily supplement dosage was considerably above MPL for nine micronutrients consumed as artificial products. Risks and possible side effects of exceeding UL by the athlete are discussed. Athletes with high energy intake may be at risk of exceeding UL of particular nutrients if multiple supplements are added. Therefore, dietary counselling of athletes should include assessment of habitual diet and nutritional supplement intake. Educating athletes to balance their diets instead of taking supplements might be prudent to prevent health risks that may occur with long-term excess nutrient intake.

Hyperammonaemia is related to both central and peripheral fatigue during exercise. Hyperammonaemia in response to exercise can be reduced through supplementation with either amino acids or combined keto analogues and amino acids (KAAA). In the present study, we determined the effect of short-term KAAA supplementation on ammonia production in subjects eating a low-carbohydrate diet who exercise. A total of thirteen male cyclists eating a ketogenic diet for 3 d were divided into two groups receiving either KAAA (KEx) or lactose (control group; LEx) supplements. Athletes cycled indoors for 2 h, and blood samples were obtained at rest, during exercise and over the course of 1 h during the recovery period. Exercise-induced ammonaemia increased to a maximum of 35 % in the control group, but no significant increase was observed in the supplemented group. Both groups had a significant increase (approximately 35 %) in uraemia in response to exercise. The resting urate levels of the two groups were equivalent and remained statistically unchanged in the KEx group after 90 min of exercise; an earlier increase was observed in the LEx group. Glucose levels did not change, either during the trial time or between the groups. An increase in lactate levels was observed during the first 30 min of exercise in both groups, but there was no difference between the groups. The present results suggest that the acute use of KAAA diminishes exercise-induced hyperammonaemia.

Ascorbic acid (vitamin C) has major effects on the intestinal uptake and utilisation of Fe in humans. The objective of the present study was to investigate the impact of Fe on the acquisition of ascorbic acid. The strategy was to study the cellular uptake and transport of ascorbic acid in the presence of Fe and also to observe the expression of the Na-dependent vitamin C transporter 1 (SVCT1) protein in human intestinal Caco-2 cells. SVCT1 is involved in the cellular uptake of ascorbic acid and is therefore a candidate for playing a role in the regulation of Fe utilisation. Caco-2 cells were cultured on transmembrane inserts in a three-compartment system followed by treatment with various combinations of FeCl2·4H2O (10–20 μmol/l) and sodium ascorbate (150 μmol/l). ELISA and Western blot analyses revealed that both SVCT1 and ferritin expressions were up-regulated in the presence of ascorbic acid in the basal compartment underneath the cells (10 and 22 %, respectively). Furthermore, when cells deficient in ascorbic acid were exposed to Fe, SVCT1 expression increased significantly (23·7 %). The increase in SVCT1 expression correlated with an increase in ascorbic acid uptake (285 %) in Fe-treated cells, as indicated by the SVCT1 inhibitor quercetin. We conclude that Fe plays an important role in regulating the uptake of ascorbic acid in human intestinal Caco-2 cells. This new angle could change the conceptual thinking of Fe and ascorbic acid utilisation and assist in the treatment and prevention of ascorbic acid-deficiency syndromes such as scurvy.

We examined the effect of dietary nicotinic acid (NA) variations before and after oxidative stress (OS) treatment on the antioxidant defence system, function and morphology of the liver along with Zn status in rats. OS was generated by three intraperitoneal injections of tert-butyl hydroperoxide in the first week for the pre-exposure group and in the third week for the post-exposure group, respectively. These groups were further divided into subgroups and fed on a diet with marginally deficient Zn (10 mg Zn/kg diet) and NA variations as NA deficient, normal and excess with 10, 30 and 1000 mg NA/kg diet, respectively. Aspartate aminotransferase and alanine aminotransferase levels were elevated in rats with OS coupled with the Zn- and NA-deficient diet, which decreased towards normal with excess dietary NA. Excess NA supplementation in the OS pre-exposure group resulted in nearly preserved hepatic architecture with normal hepatocytes, whereas maximum tissue destruction was evident in the post-exposure group with NA deficiency. Dose-dependent improvement in the antioxidant defence system, enhanced reduced glutathione levels, lowered lipid peroxidation and higher hepatic Zn levels were observed with NA supplementation. The effect was more prominent in the pre-exposure group. In conclusion, dietary NA supplementation improves hepatic Zn uptake and results in hepatoprotection against OS-induced damage in rats.

The present study investigates whether excessive fat accumulation and hyperinsulinaemia during catch-up growth on high-fat diets are altered by n-6 and n-3 PUFA derived from oils rich in either linoleic acid (LA), α-linolenic acid (ALA), arachidonic acid (AA) or DHA. It has been shown that, compared with food-restricted rats refed a high-fat (lard) diet low in PUFA, those refed isoenergetically on diets enriched in LA or ALA, independently of the n-6:n-3 ratio, show improved insulin sensitivity, lower fat mass and higher lean mass, the magnitude of which is related to the proportion of total PUFA precursors (LA+ALA) consumed. These relationships are best fitted by quadratic regression models (r2>0·8, P < 0·001), with threshold values for an impact on body composition corresponding to PUFA precursors contributing 25–30 % of energy intake. Isoenergetic refeeding on high-fat diets enriched in AA or DHA also led to improved body composition, with increases in lean mass as predicted by the quadratic model for PUFA precursors, but decreases in fat mass, which are disproportionately greater than predicted values; insulin sensitivity, however, was not improved. These findings pertaining to the impact of dietary intake of PUFA precursors (LA and ALA) and their elongated–desaturated products (AA and DHA), on body composition and insulin sensitivity, provide important insights into the search for diets aimed at counteracting the pathophysiological consequences of catch-up growth. In particular, diets enriched in essential fatty acids (LA and/or ALA) markedly improve insulin sensitivity and composition of weight regained, independently of the n-6:n-3 fatty acid ratio.

The aim of the present study was to test whether the dietary non-essential/conditionally essential amino acid composition has an effect on growth and protein utilisation and on δ13C of individual amino acids in rainbow trout (Oncorhynchus mykiss). Trout were reared on six purified diets containing only synthetic amino acids in place of protein. Diet 1 mimicked the amino acid composition of fishmeal, in diet 2, cysteine (Cys), glycine (Gly), proline (Pro) and tyrosine (Tyr) were isonitrogenously replaced by their precursor amino acids serine (Ser), glutamic acid (Glu) and phenylalanine (Phe), and in diet 3, alanine (Ala), asparagine and aspartate, Cys, Gly, Pro, Ser and Tyr were isonitrogenously replaced by Glu. Diets 4, 5 and 6 resembled diets 1, 2 and 3 except that Glu contained 0·1 % 13C-enriched Glu. A control group was reared on a fishmeal-based diet. A total of forty-two trout (4·7 (sd 0·57) g) were fed one of the diets at a level of 3·5 % body mass for 10 weeks in a flow-through system. Dietary non-essential amino acid composition significantly influenced protein gain (P < 0·025) and δ13C of Ala, arginine (Arg), Gly, histidine (His), Phe and Tyr. Non-enriched Glu was predominantly found in trout fed 13C-enriched Glu, which is consistent with the fact that Glu has been shown to be used extensively in the gut as an energy source but is less consistent with the enrichment of Pro in fish fed diet 6 compared with fish fed diet 3. Further research is required to better understand the mechanisms that lead to the alteration of amino acid δ13C between diet and body tissues.

Vegetable oils (VO) have become the predominant substitute for fish oil (FO) in aquafeeds; however, the resultant lower content of n-3 long-chain ( ≥ C20) PUFA (n-3 LC-PUFA) in fish has put their use under scrutiny. The need to investigate new oil sources exists. The present study tested the hypothesis that in Atlantic salmon (Salmo salar L.), a high intake of stearidonic acid (SDA) from Echium oil (EO) would result in increased n-3 LC-PUFA biosynthesis due to a lower requirement for Δ6 desaturase. Comparisons were made with fish fed on diets containing rapeseed oil (RO) and FO in freshwater for 112 d followed by 96 d in seawater. EO fish had higher whole-carcass SDA and eicosatetraenoic acid (ETA) in freshwater and prolonged feeding on the EO diet in seawater resulted in higher SDA, ETA, EPA and docosapentaenoic acid (DPA) compared with RO fish. Fatty acid mass balance of freshwater fish indicated higher biosynthesis of ETA and EPA in EO fish compared with fish fed on the other diets and a twofold increase in n-3 LC-PUFA synthesis compared with RO fish. In seawater, n-3 biosynthetic activity was low, with higher biosynthesis of ETA in EO fish and appearance of all desaturated and elongated products along the n-3 pathway. SDA-enriched VO are more suitable substitutes than conventional VO from a human consumer perspective due to the resulting higher SDA content, higher total n-3 and improved n-3:n-6 ratio obtained in fish, although both VO were not as effective as FO in maintaining EPA and DHA content in Atlantic salmon.

Little information is available as to whether doses of iodide similar to those recommended in clinical practice for the prevention of iodine deficiency in pregnant women affect thyroid function. The aim of the present study was to analyse whether doses of iodide can affect thyroid function in adults, and evaluate its effect on plasma markers of oxidative stress, inflammation and acute-phase proteins. A total of thirty healthy volunteers (ten men and twenty women) with normal thyroid function were randomly assigned to three groups (n 10). Each group received a daily dose of 100, 200 or 300 μg of iodide in the form of KI for 6 months. Free tetraiodothyronine (FT4) levels at day 60 of the study were higher in the groups treated with 200 and 300 μg (P = 0·01), and correlated with the increase in urinary iodine (r 0·50, P = 0·007). This correlation lost its significance after adjustment for the baseline FT4. The baseline urinary iodine and FT4 correlated positively with the baseline glutathione peroxidase. On day 60, urinary iodine correlated with C-reactive protein (r 0·461, P = 0·018), and free triiodothyronine correlated with IL-6 (r − 0·429, P = 0·025). On day 60, the changes produced in urinary iodine correlated significantly with the changes produced in α1-antitrypsin (r 0·475, P = 0·014) and ceruloplasmin (r 0·599, P = 0·001). The changes in thyroid-stimulating hormone correlated significantly with the changes in α1-antitrypsin (r − 0·521, P = 0·005) and ceruloplasmin (r − 0·459, P = 0·016). In conclusion, the administration of an iodide supplement between 100 and 300 μg/d did not modify thyroid function in a population with adequate iodine intake. The results also showed a slight anti-inflammatory and antioxidative action of iodide.

Plant polyphenols, i.e. green tea extract (GTE), possess high antioxidative and anti-inflammatory capacity, thus being protective in various models of acute inflammation. However, their anti-inflammatory effect and a feasible mechanism in haemorrhage/resuscitation (H/R)-induced liver injury remain unknown. We investigated the effects of GTE and the role of NF-κB in the pathogenesis of liver injury induced by H/R, and their effects on intercellular adhesion molecule-1 (ICAM-1) expression and neutrophil infiltration. Female Lewis rats were fed a standard chow diet (control, ctrl) or a diet containing 0·1 % polyphenolic GTE for five consecutive days before H/R. Rats were haemorrhaged to a mean arterial pressure of 30 (sem 2) mmHg for 60 min and resuscitated. Control groups (sham_ctrl and sham_GTE) underwent surgical procedures without H/R. At 2 h after resuscitation, tissues were harvested. Serum alanine aminotransferase (ALT) and IL-6 were measured. Hepatic necrosis, ICAM-1 expression and polymorphonuclear leucocyte (PMNL) infiltration were assessed. Hepatic expression of IκBα (phospho) was measured. H/R induced strong liver damage with increased necrosis and serum ALT levels. Compared with both sham groups, inflammatory markers (serum IL-6 and hepatic PMNL infiltration) were elevated after H/R (P < 0·05). Also, H/R increased IκBα phosphorylation. GTE administration markedly (P < 0·05) decreased serum ALT and IL-6 levels, hepatic necrosis as well as PMNL infiltration and the expression of ICAM-1 and phosphorylated IκBα compared with H/R. In conclusion, we observed that NF-κB activation plays an important role in the pathogenesis of liver injury after H/R through the up-regulation of hepatic ICAM-1 expression and subsequent PMNL infiltration. GTE pre-treatment prevents liver damage in this model of acute inflammation through a NF-κB-dependent mechanism.

Several mechanisms have been proposed for the positive health effects associated with dietary consumption of long-chain n-3 PUFA (n-3 LC-PUFA) including DHA (22 : 6n-3) and EPA (20 : 5n-3). After dietary intake, LC-PUFA are incorporated into membranes and can be converted to their corresponding N-acylethanolamines (NAE). However, little is known on the biological role of these metabolites. In the present study, we tested a series of unsaturated NAE on the lipopolysaccharide (LPS)-induced NO production in RAW264.7 macrophages. Among the compounds tested, docosahexaenoylethanolamine (DHEA), the ethanolamide of DHA, was found to be the most potent inhibitor, inducing a dose-dependent inhibition of NO release. Immune-modulating properties of DHEA were further studied in the same cell line, demonstrating that DHEA significantly suppressed the production of monocyte chemotactic protein-1 (MCP-1), a cytokine playing a pivotal role in chronic inflammation. In LPS-stimulated mouse peritoneal macrophages, DHEA also reduced MCP-1 and NO production. Furthermore, inhibition was also found to take place at a transcriptional level, as gene expression of MCP-1 and inducible NO synthase was inhibited by DHEA. To summarise, in the present study, we showed that DHEA, a DHA-derived NAE metabolite, modulates inflammation by reducing MCP-1 and NO production and expression. These results provide new leads in molecular mechanisms by which DHA can modulate inflammatory processes.

To establish the effectiveness of a new phytosterol-containing spread derived from rice bran oil (RBO), a randomised, double-blind, cross-over human clinical trial was conducted over 12 weeks. A total of eighty mildly hypercholesterolaemic (total blood cholesterol level ≥ 5 and ≤ 7·5 mmol/l with a serum TAG level of ≤ 4·5 mmol/l) individuals were randomised into two groups (n 40). Group 1 consumed spread only daily for 4 weeks. They were randomised to consume 20 g RBO spread (RBOS), 20 g standard spread (SS) or 20 g phytosterol-enriched spread (PS). After a 4-week period, individuals changed to the next randomised treatment until all three treatments had been consumed. Group 2 consumed spread plus oil daily for 4 weeks. They consumed 20 g RBOS plus 30 ml RBO, 20 g SS plus 30 ml sunflower oil or 20 g RBOS. Blood samples were collected for the analysis of lipid parameters, and 3 d diet records were collected. Compared with SS, RBOS significantly reduced total cholesterol by 2·2 % (P = 0·045), total cholesterol:HDL by 4·1 % (P = 0·005) and LDL-cholesterol by 3·5 % (P = 0·016), but was not as effective overall as PS, which reduced total cholesterol by 4·4 % (P = 0·001), total cholesterol:HDL by 3·4 % (P = 0·014) and LDL-cholesterol by 5·6 % (P = 0·001). In group 2, the addition of RBO to the RBOS produced no differences in cholesterol levels. These results confirm that RBOS is effective in lowering serum cholesterol when consumed as part of a normal diet.

Vitamin A treatment reduces mortality during acute measles infection, and vitamin A supplementation (VAS) to children above 6 months of age may reduce the incidence of measles infection. The effect of VAS at birth on measles incidence is unknown. In a randomised placebo-controlled trial in Guinea-Bissau, normal-birth-weight newborns were randomised to 50 000 IU (15 mg) VAS or placebo. During the trial, a measles epidemic occurred. We linked data from the trial with data from the measles infection surveillance and studied the effect of VAS on the measles incidence before 12 months of age in both sexes. A total of 165 measles cases were identified among the 4183 children followed from 28 d of age. Up to 6 months of age, the incidence rate ratio of measles for VAS compared with placebo was 0·54 (95 % CI 0·25, 1·15) among boys and 1·57 (95 % CI 0·80, 3·08) among girls (test of interaction, P = 0·04). The corresponding figures at 12 months were 0·67 (95 % CI 0·43, 1·05) and 1·17 (95 % CI 0·76, 1·79) (test of interaction, P = 0·08). VAS compared with placebo tended to be associated with less measles hospitalisation or death during the first 6 months of life in boys (P = 0·06), but not in girls. VAS at birth may affect the susceptibility to measles infection during the first 6 months of life in a sex-differential manner.

Intervention studies have demonstrated that saturated fat increases total and LDL-cholesterol concentrations, and it is therefore recommended that the intake of high-fat dairy products be limited. However, observational studies have found an inverse relationship between the intake of dairy products and incidence of CVD. We aimed to study whether the Ca content of dairy products influences the effect of dairy fat on the lipid profile. The study had a randomised cross-over design. Subjects (n 9) were randomised to one of the sequence of four isoenergetic 10 d diets: low Ca and low fat (LC/LF: approximately 700 mg Ca/d, 25 % of energy (fat); high Ca and LF (HC/LF: approximately 2800 mg Ca/d, 25 % of energy fat); LC and high fat (LC/HF: approximately 700 mg Ca/d, 49 E% fat); or HC and HF (approximately 2800 mg Ca/d, 49 E% fat). Blood variables were measured before and after each diet period, and faeces and urine were collected at the end of each diet period. A two-way ANOVA was used to examine the effect of Ca and fat intake. Independent of Ca intake, the HF diet increased the concentrations of total (9 %; P < 0·0001), LDL (14 %; P < 0·0001)- and HDL (13 %; P = 0·0002)-cholesterol compared with the LF diet. However, independent of fat intake, the HC diet decreased the concentrations of total (4 %; P = 0·0051) and LDL-cholesterol (10 %; P < 0·0001) but not HDL-cholesterol compared with the LC diet. In addition, total:HDL-cholesterol was decreased (5 %; P = 0·0299), and HDL:LDL was increased (12 %; P = 0·0097) by the HC diet compared with the LC diet. Faecal fat excretion was increased by both the HC (P < 0·0001) and HF (P = 0·0052) diets. In conclusion, we observed that dairy Ca seems to partly counteract the raising effect of dairy fat on total and LDL-cholesterol, without reducing HDL-cholesterol.

Poor physical fitness is associated with increased health-related risks in children. The association of nutritional status indicators and physical fitness in children residing in developing countries is not well characterised. We conducted a cross-sectional study among 1945 children of age 5–12 years in Bogotá, Colombia, to assess whether anthropometric and micronutrient status indicators were associated with performance in the shuttle run and standing long jump tests. Stunted children scored significantly lower in the run (0·4 s; P = 0·0002) and jump (6 cm; boys only; P = 0·003) tests than non-stunted children, after adjustment for age and other factors. Children who were thin, overweight or obese ran slower than normal-weight children (P < 0·01). Lower jump scores were associated with overweight or obesity and greater arm fat area in boys only (P < 0·0001). Girls with low ferritin concentrations ran 0·6 s slower than girls with normal ferritin concentrations (P = 0·02). Erythrocyte folate concentrations were linearly related to higher run (P < 0·0001) and long jump scores (P = 0·0001). Boys with marginal or low vitamin B12 status had 4 cm lower long jump scores than children with normal status (P = 0·01). Suboptimal anthropometric and micronutrient status are related to poorer performance in fitness tests. The effects of improving nutritional status on physical fitness of children warrant investigation.

Intestinal bacterial colonisation in pre-term infants is delayed compared with full-term infants, leading to an increased risk of gastrointestinal disease. Modulation of colonisation through dietary supplementation with probiotics or prebiotics could decrease such a risk. The present study evaluated clinical tolerance, the effects on gut microbiota, and inflammatory and immunological mucosal responses to an infant formula adapted for pre-term infants that included in its manufacturing process a fermentation step with two probiotic strains, Bifidobacterium breve C50 and Streptococcus thermophilus 065, inactivated by heat at the end of the process. A total of fifty-eight infants (gestational age: 30–35 weeks), fed either the fermented pre-term formula or a standard pre-term formula, were followed up during their hospital stay. Clinical tolerance, faecal microbiota using a culture and a culture-independent method (temporal temperature gel electrophoresis), faecal calprotectin and secretory IgA were analysed weekly. No difference was observed regarding anthropometric data and digestive tolerance, except for abdominal distension, the incidence of which was lower in infants fed the fermented formula for 2 weeks. Bacterial colonisation was not modified by the type of feeding, particularly for bifidobacteria. Faecal calprotectin was significantly lower in infants fed the fermented formula for 2 weeks, and secretory IgA increased with both mother's milk and the fermented formula. The fermented formula was well tolerated and did not significantly modulate the bacterial colonisation but had benefits on inflammatory and immune markers, which might be related to some features of gastrointestinal tolerance.

Recent findings indicate that household food insecurity affects children's social skill development in the early years of elementary school. It is important to assess the persistency of developmental consequences and investigate whether all categories of social skills are equally affected by food insecurity experiences. The present paper estimates population-averaged and subject-specific models for children's social skill scores reported by school teachers using longitudinal data on 2310 boys and 2400 girls in the USA enrolled in the 1st (aged 6–9 years), 3rd (aged 8–11 years) and 5th (aged 10–13 years) grades (1999–2003) from the Early Childhood Longitudinal Study-Kindergarten. The main findings are, first, significantly (P < 0·05) negative, contemporaneous and transitional relationships between food insecurity experiences and children's social skill scores are evident. Estimates based on sex-stratified samples indicate that the contemporaneous association is strongest among girls, while the association of an early transition from food insecurity in the 1st grade to food security in the 3rd grade is strongest among boys. Second, food insecurity experiences predict children's social skill scores emphasising self-control, attentiveness and task persistence, rather than interpersonal relationships or externalising behaviour. Overall, the findings underscore the multifaceted effect that household food insecurity has on children's social skills and provide the strongest empirical evidence to date that the experiences are linked with non-nutritional developmental consequences for children over a time horizon spanning several years.