The North American Institute of Medicine (IOM) recently published their report on dietary reference intakes (DRI) for Ca and vitamin D. The DRI committee's deliberations underpinning this most comprehensive report on vitamin D nutrition to date benefited hugely from a much expanded knowledge base in vitamin D over the last decade or more. However, since their release, the vitamin D DRI have been the subject of intense controversy, which is largely due to the persistence of fundamental knowledge gaps in vitamin D. These can be identified at the levels of exposure, metabolism, storage, status, dose–response, function and beneficial or adverse health effects, as well as safe and effective application of intake recommendations at the population level through sustainable food-based approaches. The present review provides a brief overview of the approach used by the IOM committee to revise the DRI for vitamin D and to collate from a number of authoritative sources key knowledge gaps in vitamin D nutrition from the public health perspective. A number of research topics are outlined and data requirements within these are identified and mapped to the risk assessment framework used by the DRI committee. While not intended as an exhaustive list, it provides a basis for organising and prioritising research efforts in the area of vitamin D, which may offer a perspective on the major areas in need of attention. It is intended to be of use to researchers, national policy makers, the public health community, industry groups and other relevant stakeholders including funding institutions.

Vitamins C and E can act as potent antioxidants to reduce the damage caused by reactive oxygen species in gastric mucosa. Whether vitamin supplements for Helicobacter pylori eradication regimen could improve the rate of eradication remains uncertain. Therefore, we performed a meta-analysis to evaluate the efficacy of vitamins C and E supplementation for the eradication of H. pylori. Searches were conducted in the databases PubMed, EMBASE and Cochrane Library. Randomised controlled trials (RCT) that fulfilled the inclusion criteria and addressed the clinical questions of this analysis were further assessed. Of the six RCT included, five had a low methodological quality. Of the six RCT, three compared the efficacy of the eradication regimen v. eradication regimen plus vitamins C and E. The result of the meta-analysis showed a non-significant difference in the eradication rate of H. pylori between the two groups (risk ratio (RR) 0·93, P = 0·76). Another three RCT compared the eradication regimen v. eradication regimen plus vitamin C only, and there too there was no significant difference in the eradication rate (RR 0·83, P = 0·32). In conclusion, vitamins C and/or E supplements to the H. pylori eradication regimen could not improve the eradication rate. However, currently available data do not draw a definitive conclusion about the effectiveness of antioxidant vitamins on H. pylori eradication, owing to the small sample size and low-to-moderate methodological quality.

The present study used a systematic review approach to identify relevant randomised control trials (RCT) with vitamin D and then apply meta-regression to explore the most appropriate model of the vitamin D intake–serum 25-hydroxyvitamin D (25(OH)D) relationship to underpin setting reference intake values. Methods included an updated structured search on Ovid MEDLINE; rigorous inclusion/exclusion criteria; data extraction; and meta-regression (using different model constructs). In particular, priority was given to data from winter-based RCT performed at latitudes >49·5°N (n 12). A combined weighted linear model meta-regression analyses of natural log (Ln) total vitamin D intake (i.e. diet and supplemental vitamin D) v. achieved serum 25(OH)D in winter (that used by the North American Dietary Reference Intake Committee) produced a curvilinear relationship (mean (95 % lower CI) serum 25(OH)D (nmol/l) = 9·2 (8·5) Ln (total vitamin D)). Use of non-transformed total vitamin D intake data (maximum 1400 IU/d; 35 μg/d) provided for a more linear relationship (mean serum 25(OH)D (nmol/l) = 0·044 × (total vitamin D)+33·035). Although inputting an intake of 600 IU/d (i.e. the RDA) into the 95 % lower CI curvilinear and linear models predicted a serum 25(OH)D of 54·4 and 55·2 nmol/l, respectively, the total vitamin D intake that would achieve 50 (and 40) nmol/l serum 25(OH)D was 359 (111) and 480 (260) IU/d, respectively. Inclusion of 95 % range in the model to account for inter-individual variability increased the predicted intake of vitamin D needed to maintain serum 25(OH)D ≥ 50 nmol/l to 930 IU/d. The model used to describe the vitamin D intake–status relationship needs to be considered carefully when setting new reference intake values in the Europe.

Epidemiological studies of dietary glycaemic index (GI) and glycaemic load (GL) in relation to diabetes risk have yielded inconsistent results. We aimed to examine the associations between dietary GI and GL and the risk of type 2 diabetes by conducting a meta-analysis of prospective cohort studies. Relevant studies were identified by a PubMed database search up to February 2011. Reference lists from retrieved articles were also reviewed. We included prospective cohort studies that reported risk estimates with 95 % CI for the associations between dietary GI and GL and the risk of type 2 diabetes. Either a fixed- or random-effects model was used to compute the summary relative risk (RR). We identified thirteen prospective cohort studies of dietary GI or GL related to diabetes risk. The summary RR of type 2 diabetes for the highest category of the GI compared with the lowest was 1·16 (95 % CI 1·06, 1·26; n 12), with moderate evidence of heterogeneity (P = 0·02, I2 = 50·8 %). For the GL, the summary RR was 1·20 (95 % CI 1·11, 1·30; n 12), with little evidence of heterogeneity (P = 0·10, I2 = 34·8 %). No evidence of publication bias was observed. In addition, the associations persisted and remained statistically significant in the sensitivity analyses. In conclusion, the present meta-analysis provides further evidence in support of significantly positive associations between dietary GI and GL and the risk of type 2 diabetes. Reducing the intake of high-GI foods may bring benefits in diabetes prevention.

Waste from agricultural products represents a disposal liability, which needs to be addressed. Palm oil is the most widely traded edible oil globally, and its production generates 85 million tons of aqueous by-products annually. This aqueous stream is rich in phenolic antioxidants, which were investigated for their composition and potential in vitro biological activity. We have identified three isomers of caffeoylshikimic acid as major components of oil palm phenolics (OPP). The 2,2-diphenyl-1-picrylhydrazyl assay confirmed potent free radical scavenging activity. To test for possible cardioprotective effects of OPP, we carried out in vitro LDL oxidation studies as well as ex vivo aortic ring and mesenteric vascular bed relaxation measurements. We found that OPP inhibited the Cu-mediated oxidation of human LDL. OPP also promoted vascular relaxation in both isolated aortic rings and perfused mesenteric vascular beds pre-contracted with noradrenaline. To rule out developmental toxicity, we performed teratological studies on rats up to the third generation and did not find any congenital anomalies. Thus, these initial studies suggest that OPP is safe and may have a protective role against free radical damage, LDL oxidation and its attendant negative effects, as well as vascular constriction in mitigating atherosclerosis. Oil palm vegetation liquor thus represents a new source of phenolic bioactives.

It is well established that plant phenolics elicit various biological activities, with positive effects on health. Palm oil production results in large volumes of aqueous by-products containing phenolics. In the present study, we describe the effects of oil palm phenolics (OPP) on several degenerative conditions using various animal models. OPP reduced blood pressure in a NO-deficient rat model, protected against ischaemia-induced cardiac arrhythmia in rats and reduced plaque formation in rabbits fed an atherogenic diet. In Nile rats, a spontaneous model of the metabolic syndrome and type 2 diabetes, OPP protected against multiple aspects of the syndrome and diabetes progression. In tumour-inoculated mice, OPP protected against cancer progression. Microarray studies on the tumours showed differential transcriptome profiles that suggest anti-tumour molecular mechanisms involved in OPP action. Thus, initial studies suggest that OPP may have potential against several chronic disease outcomes in mammals.

The objective of the present study was to investigate age-related differences in erythrocyte membrane fluidity (EMF) and changes in antioxidant capacity following supplementation. A total of seventy-four children were randomly divided into two groups: group A1 was the placebo-controlled group and group A2 was supplemented daily with 600 μg retinol, 1·0 mg β-carotene, 100 mg tocopherol, 300 mg ascorbic acid and 200 μg Se. A total of ninety young people were randomly divided into B1 and B2 groups, and ninety-one elderly subjects were divided into C1 and C2 groups. Groups B1 and C1 were placebo-controlled groups, and groups B2 and C2 were daily supplemented with 900 μg retinol, 1·5 mg β-carotene, 200 mg tocopherol, 500 mg ascorbic acid and 400 μg Se. Results showed that plasma malondialdehyde (MDA) was 5·35 μmol/l in children, which was lower than in young and elderly people. The MDA levels of the young and elderly individuals in the treated groups were significantly lower compared with the control groups, but the supplementation did not alter MDA levels in children. At baseline, there was a lower value of polarisation (ρ) and microviscosity (η) in children, indicating a higher EMF, than in both the young and elderly subjects. After the 2-month trial, the ρ and η values of young and elderly subjects in the treated groups decreased significantly in comparison with the placebo groups, indicating an increase in EMF. In conclusion, there was a background of higher MDA levels and lower EMF in young and elderly people than in children, which could be improved by antioxidant supplementation.

Sarcopenia is defined as age-related loss of muscle mass and strength. Energy restriction (ER) delays fibre loss by limiting the accumulated deleterious effects of reactive oxygen species on muscle. However, insufficient protein intake during ER might affect muscle mass and function. We hypothesised that ingestion of fast-digested proteins such as whey protein (WP) improves muscle protein synthesis and muscle strength in aged ER rats. The effect of WP or casein (CAS, slow protein) on muscle mass, protein synthesis and strength was evaluated in 21-month-old rats fed for 5 months either ad libitum (AL) or a 40 % protein and energy-restricted (PER) or 40 % AL-isonitrogenous ER diet. The nitrogen balance was reduced in PER-CAS rats only ( − 48 % v. AL-CAS). WP stimulated muscle protein synthesis rates compared with CAS in all groups (+21,+37 and +34 % in AL, PER and ER conditions, respectively). Muscle strength was higher in ER rats than in AL rats (+23 and +12 % for WP or CAS, respectively). Muscle performance tended to be greater in ER rats fed WP than in ER-CAS rats (P < 0·09). In conclusion, we observed that long-term ER combined with maintained protein intake had a beneficial impact on muscle protein synthesis rate and function during ageing.

Phenolic compounds are one of the main reasons behind the healthy properties of virgin olive oil (VOO). However, their daily intake from VOO is low compared with that obtained from other phenolic sources. Therefore, the intake of VOO enriched with its own phenolic compounds could be of interest to increase the daily dose of these beneficial compounds. To evaluate the effectiveness of enrichment on their bioavailability, the concentration of phenolic compounds and their metabolites in human plasma (0, 60, 120, 240 and 300 min) from thirteen healthy volunteers (seven men and six women, aged 25 and 69 years) was determined after the ingestion of a single dose (30 ml) of either enriched virgin olive oil (EVOO) (961·17 mg/kg oil) or control VOO (288·89 mg/kg oil) in a cross-over study. Compared with VOO, EVOO increased plasma concentration of the phenol metabolites, particularly hydroxytyrosol sulphate and vanillin sulphate (P < 0·05). After the consumption of VOO, the maximum concentration of these peaks was reached at 60 min, while EVOO shifted this maximum to 120 min. Despite these differences, the wide variability of results indicates that the absorption and metabolism of olive oil phenols are highly dependent on the individual.

Energetic efficiency was evaluated in composite bred heifers born from dams receiving 1·8 or 1·2 kg/d winter supplementation for approximately 80 d before parturition. Heifers were then developed post-weaning and randomly assigned to heifer development treatments of either control (100 %; ad libitum; n 8/year) or restricted (80 %; fed 80 % of supplementation fed to controls adjusted to a common body weight: n 8/year) in a 2-year study. A glucose tolerance test (GTT) and acetate irreversible loss test (AILT) were administered to heifers at the termination of a 140 d development period when the heifers were approximately 403 d of age and consumed a silage-based diet, and again at 940 d of age when pregnant with their second calf and grazing dormant forage. No differences were measured (P>0·08) for dam winter nutrition or heifer development treatment for baseline serum metabolites or measures in either the GTT or the AILT. However, changes in baseline serum concentrations (P>0·05) were different between metabolic challenges, which occurred at different stages of development. No difference in acetate disappearance (P = 0·18) and half-life (P = 0·66) was measured between the two metabolic challenges. A trend for glucose half-life to be shorter in heifers born from dams receiving in utero winter treatments that supplied 1·2 kg/d of winter supplementation was observed (P = 0·083). Heifers developed with lower total DM intake during a 140 d development period had similar glucose and acetate incorporation rates as ad libitum-fed heifers when evaluated at two different production stages.

Naringin, a bioflavonoid isolated from grapefruit, is well known to possess lipid-lowering and insulin-like properties. Therefore, we assessed whether naringin treatment ameliorates insulin resistance (IR), β-cell dysfunction, hepatic steatosis and kidney damage in high-fat diet (HFD)–streptozotocin (STZ)-induced type 2 diabetic rats. Wistar albino male rats were fed a HFD (55 % energy from fat and 2 % cholesterol) to develop IR and on the 10th day injected with a low dose of streptozotocin (40 mg/kg, intraperitoneal (ip)) to induce type 2 diabetes. After confirmation of hyperglycaemia (>13·89 mmol/l) on the 14th day, different doses of naringin (25, 50 and 100 mg/kg per d) and rosiglitazone (5 mg/kg per d) were administered orally for the next 28 d while being maintained on the HFD. Naringin significantly decreased IR, hyperinsulinaemia, hyperglycaemia, dyslipidaemia, TNF-α, IL-6, C-reactive protein and concomitantly increased adiponectin and β-cell function in a dose-dependent manner. Increased thiobarbituric acid-reactive substances and decreased antioxidant enzyme activities in the serum and tissues of diabetic rats were also normalised. Moreover, naringin robustly increased PPARγ expression in liver and kidney; phosphorylated tyrosine insulin receptor substrate 1 in liver; and stress proteins heat shock protein (HSP)-27 and HSP-72 in pancreas, liver and kidney. In contrast, NF-κB expression in these tissues along with sterol regulatory element binding protein-1c and liver X receptor- expressions in liver were significantly diminished. In addition, microscopic observations validated that naringin effectively rescues β-cells, hepatocytes and kidney from HFD-STZ-mediated oxidative damage and pathological alterations. Thus, this seminal study provides cogent evidence that naringin ameliorates IR, dyslipidaemia, β-cell dysfunction, hepatic steatosis and kidney damage in type 2 diabetic rats by partly regulating oxidative stress, inflammation and dysregulated adipocytokines production through up-regulation of PPARγ, HSP-27 and HSP-72.

Hepatitis C virus (HCV) infection is associated with oxidative stress and vitamin A possesses antioxidant activity. The objective of the present study was to investigate vitamin A nutritional status in chronic hepatitis, liver cirrhosis and hepatocellular carcinoma (HCC), according to biochemical, functional and dietetic indicators correlating these findings with liver function, liver damage and death. Vitamin A nutritional status was analysed by serum retinol levels, dietetic indicators and functional indicators. A total of 140 patients with HCV-related liver disease were enrolled. Vitamin A deficiency was detected in 54·3 % of all patients, and there was a progressive drop in serum retinol levels from chronic hepatitis C patients towards cirrhosis and HCC patients. Increased total bilirubin, liver transaminases and prothrombin time, presence of hepatic encephalopathy and ascites were related to reduced serum retinol levels, and values ≤ 0·78 μmol/l of serum retinol were associated with liver-related death. A high prevalence of inadequate intake of vitamin A was observed in all stages of chronic liver disease. The functional indicator was not an adequate parameter for evaluating the vitamin A nutritional status. Therefore, serum retinol concentration is related to severity of the disease, liver complications and mortality. The effectiveness of nutritional counselling and measures of intervention in this group in improving vitamin A nutritional status should be examined further in a controlled study.

The addition of carbohydrate to drinks designed to have a role in rehydrating the body is commonplace. The gastric emptying and fluid uptake characteristics following repeated ingestion of drinks with high and low glucose concentrations were examined in eight subjects (three male and five female). Following a 13 h fluid restriction period, the subjects ingested a volume of test solution amounting to 3 % of the initial body mass over a period of 60 min. Test drinks were 2 and 10 % glucose–electrolyte solutions with osmolalities of 189 (sd 3) and 654 (sd 3) mOsm/kg, respectively. The initial bolus of each test solution contained 10 g of 2H2O. Blood samples were collected throughout drinking and for 60 min afterwards. Gastric volumes were determined via gastric aspiration at 15 min intervals for 120 min. No difference between trials in total stomach volume was observed until 30 min after the ingestion of the first bolus of test drink, but blood 2H concentration was increased during both trials 10 min after ingestion of the first bolus. Blood 2H concentration was greater at this time point during the 2 % glucose trial than during the 10 % glucose trial and remained higher for the duration of the trial with the exception of one time point. Urine volume at the end of the trial was greater in the 2 % glucose trial than in the 10 % glucose trial. It is concluded that the reduced overall rate of fluid uptake following ingestion of the 10 % glucose solution was due largely to a relatively slow rate of gastric emptying.

The objective of the present study was to assess the effect of adding specific prebiotics to standard formula feeding on the number of fever episodes in the first year of life. In the present randomised, double-blind, placebo-controlled trial in seven centres in five West European countries, 830 healthy term infants, without a first-degree family history of allergic disease, of mothers who indicated to give only formula feeding were randomised either to receive a standard non-hydrolysed cows' milk-based formula to which a mixture of specific oligosaccharides was added (prebiotics group (PG)), or to receive a similar formula without oligosaccharides (control group (CG)). A separate reference group consisted of 300 breast-fed infants. The primary outcome was the number of fever episodes prospectively documented by the parents. There was no difference in the number of fever episodes between the PG (median value 1·19; 25th–75th percentile 0·09–2·34) and CG (1·16; 25th–75th percentile 0·06–2·38). The median number of fever episodes in the separate breast-feeding reference group was 1·24 (25th–75th percentile 0·51–3·45). There was no effect of adding specific prebiotics to standard formula feeding in reducing the number of fever episodes in the present study.

Worldwide, the iodisation of salt has clearly improved iodine status. In industrialised countries, iodised salt added to processed food contributes most to iodine supply. Yet it is unclear as to what extent changes in the latter may affect the iodine status of populations. Between 2004 and 2009, 24-h urinary iodine excretions (UIE) were repeatedly measured in 278 German children (6 to 12 years old) of the Dortmund Nutritional and Anthropometric Longitudinally Designed Study (n 707). Na excretion measurements and simultaneously collected 3-d weighed dietary records provided data on intakes of the most important dietary sources of iodine in the children's diet. Actual trends of UIE (2004–9) and contributions of relevant food groups were analysed by mixed linear regression models. Longitudinal regression analysis showed a plateau of UIE in 2004–6; afterwards, UIE significantly decreased till 2009 (P = 0·01; median 24-h UIE in 2004–6: 85·6 μg/d; 2009: 80·4 μg/d). Median urinary iodine concentration fell below the WHO criteria for iodine sufficiency of 100 μg/l in 2007–9. Salt, milk, fish and egg intake (g/d) were significant predictors of UIE (P < 0·005); and the main sources of iodine were salt and milk (48 and 38 %, respectively). The present data hint at a beginning deterioration in the iodine status of German schoolchildren. A decreased use of iodised salt in industrially produced foods may be one possible reason for this development. Because of the generally known risks for cognitive impairment due to even mild iodine deficits in children, a more widespread use of iodised salt, especially in industrially processed foods, has to be promoted.

In rats, oligofructose has been shown to stimulate satiety hormone secretion, reduce energy intake and promote weight loss. The present study aimed to examine the effect of oligofructose supplementation on appetite profiles, satiety hormone concentrations and energy intake in human subjects. A total of thirty-one healthy subjects (ten men and twenty-one women) aged 28 (sem 3) years with a BMI of 24·8 (sem 0·3) kg/m2 were included in a randomised double-blind, cross-over study. The subjects received 10 g oligofructose, 16 g oligofructose or 16 g placebo (maltodextrin) daily for 13 d, with a 2-week washout period between treatments. Appetite profile, active glucagon-like peptide 1 (GLP-1) and peptide YY3-36 (PYY) concentrations and energy intake were assessed on days 0 and 13 of the treatment period. Time × treatment interaction revealed a trend of reduction in energy intake over days 0–13 by oligofructose (P = 0·068). Energy intake was significantly reduced (11 %) over time on day 13 compared with day 0 with 16 g/d oligofructose (2801 (sem 301) v. 3217 (sem 320) kJ, P < 0·05). Moreover, energy intake was significantly lower with 16 g/d oligofructose compared with 10 g/d oligofructose on day 13 (2801 (sem 301) v. 3177 (sem 276) kJ, P < 0·05). Area under the curve (AUC) for GLP-1 on day 13 was significantly higher with 16 g/d oligofructose compared with 10 g/d oligofructose (45 (sem 4) v. 41 (sem 3) pmol/l × h, P < 0·05). In the morning until lunch, AUC0–230 min for PYY on day 13 was significantly higher with 16 g/d oligofructose compared with 10 g/d oligofructose and placebo (409 (sem 35) v. 222 (sem 19) and 211 (sem 20) pg/ml × h, P < 0·01). In conclusion, 16 g/d and not 10 g/d oligofructose may be an effective dose to reduce energy intake, possibly supported by higher GLP-1 and PYY concentrations.