Direct observation(s) of energy intake (EI) via buffet meals served in the laboratory are often carried out within short-term exercise intervention studies. The reproducibility of values obtained has not been assessed either under resting control conditions or post-exercise, in overweight and obese females. A total of fourteen sedentary, pre-menopausal females (BMI 30·0 (sd 5·1) kg/m2) completed four trials; two exercise and two control. Each trial lasted 24 h spanning over 2 d; conducted from afternoon on day 1 and morning on day 2. An exercise session to expend 1·65 MJ was completed on day 1 of exercise trials, and three buffet meals were served during each trial. Reproducibility of post-exercise changes in energy and macronutrient intakes was assessed at each individual buffet meal by intraclass correlation coefficient (ri). Only the ri values for post-exercise changes in energy (ri 0·44 (95 % CI − 0·03, 0·77), P = 0·03) and fat intake (ri 0·51 (95 % CI 0·04, 0·81), P = 0·02) at the lunch buffet meal achieved statistical significance; however, these ri values were weak and had large associated 95 % CI, which indicates a large degree of variability associated with these measurements. Energy and macronutrient intakes at the breakfast and evening buffet meals were not reproducible. This study concludes that the frequently used laboratory-based buffet meal method of assessing EI does not produce reliable, reproducible post-exercise changes in EI in overweight and obese women.

The present study was conducted to test the hypothesis that dietary arginine promotes digestion and absorption capacity, and, thus, enhances fish growth. This improvement might be related to the target of rapamycin (TOR) and eIF4E-binding protein (4E-BP). A total of 1200 juvenile Jian carp, Cyprinus carpio var. Jian, with an average initial weight of 6·33 (se 0·03) g, were fed with diets containing graded concentrations of arginine, namely, 9·8 (control), 12·7, 16·1, 18·5, 21·9 and 24·5 g arginine/kg diet for 9 weeks. An real-time quantitative PCR analysis was performed to determine the relative expression of TOR and 4E-BP in fish muscle, hepatopancreas and intestine. Dietary arginine increased (P < 0·05): (1) glutamate-oxaloacetate transaminase and glutamate-pyruvate transaminase activities in muscle and hepatopancreas; (2) intestine and hepatopancreas protein content, folds height, and trypsin, chymotrypsin, lipase, Na+/K+-ATPase, alkaline phosphatase, γ-glutamyl transpeptidase and creatine kinase activities in intestine; (3) Lactobacillus counts; (4) relative expression of TOR in the muscle, hepatopancreas and distal intestine (DI); (5) relative expression of 4E-BP in proximal intestine (PI) and mid-intestine (MI), as compared with the control group. In contrast, dietary arginine reduced (P < 0·05): (1) plasma ammonia content; (2) Aeromonas hydrophila and Escherichia coli counts; (3) relative expression of TOR in PI and MI; (4) relative expression of 4E-BP in the muscle, hepatopancreas and DI. The arginine requirement estimated by specific growth rate using quadratic regression analysis was found to be 18·0 g/kg diet. These results indicate that arginine improved fish growth, digestive and absorptive ability and regulated the expression of TOR and 4E-BP genes.

Proanthocyanidins have been shown to improve postprandial hypertriacylglycerolaemia. The present study aims to determine the actual contribution of chylomicrons (CM) and VLDL in the hypotriacylglycerolaemic action of grape seed proanthocyanidin extract (GSPE) in the postprandial state and to characterise the mechanisms by which the GSPE treatment reduces TAG-rich lipoproteins in vivo. A plasma lipid tolerance test was performed on rats fasted for 14 h and orally loaded with lard containing either GSPE or not. GSPE (250 mg/kg body weight) markedly blocked the increase in plasma TAG induced by lard, with a statistically significant reduction of 22 % in the area under the curve. The VLDL-rich fraction was the major contributor (72 %) after 1 h, whereas the CM-rich fraction was the major contributor (85 %) after 3 h. At 5 and 7 h after treatment, CM-rich and VLDL-rich fractions showed a similar influence. Plasma post-heparin lipoprotein lipase (LPL) activity and LPL mRNA levels in white adipose tissue and muscle were not affected by GSPE. On the contrary, GSPE treatment significantly repressed (30 %) the secretion of VLDL-TAG. In the liver, GSPE treatment induced different effects on the expression of acyl-coenzyme A synthetase long-chain family member 1, Apoc3 and 3-hydroxy-3-methylglutaryl-coenzyme A reductase at 1 h and Cd36 at 5 h, compared to those induced by lard. Furthermore, GSPE treatment significantly increased the activity of carnitine palmitoyltransferase 1a at 1 h. In conclusion, both CM-rich and VLDL-rich fractions contributed to the hypotriacylglycerolaemic action of GSPE, but their influence depended on time. GSPE induces hypotriacylglycerolaemic actions by repressing lipoprotein secretion and not by increasing LPL activity.

Renewed interest in alternative medicine among diabetic individuals prompted us to investigate anti-diabetic effects of Morinda citrifolia (noni) in high-fat diet (HFD)-fed mice. Type 2 diabetes is associated with increased glucose production due to the inability of insulin to suppress hepatic gluconeogenesis and promote glycolysis. Insulin inhibits gluconeogenesis by modulating transcription factors such as forkhead box O (FoxO1). Based on microarray analysis data, we tested the hypothesis that fermented noni fruit juice (fNJ) improves glucose metabolism via FoxO1 phosphorylation. C57BL/6 male mice were fed a HFD and fNJ for 12 weeks. Body weights and food intake were monitored daily. FoxO1 expression was analysed by real-time PCR and Western blotting. Specificity of fNJ-associated FoxO1 regulation of gluconeogenesis was confirmed by small interfering RNA (siRNA) studies using human hepatoma cells, HepG2. Supplementation with fNJ inhibited weight gain and improved glucose and insulin tolerance and fasting glucose in HFD-fed mice. Hypoglycaemic properties of fNJ were associated with the inhibition of hepatic FoxO1 mRNA expression, with a concomitant increase in FoxO1 phosphorylation and nuclear expulsion of the proteins. Gluconeogenic genes, phosphoenolpyruvate C kinase (PEPCK) and glucose-6-phosphatase (G6P), were significantly inhibited in mice fed a HFD+fNJ. HepG2 cells demonstrated more than 80 % inhibition of PEPCK and G6P mRNA expression in cells treated with FoxO1 siRNA and fNJ. These data suggest that fNJ improves glucose metabolism via FoxO1 regulation in HFD-fed mice.

Intestinal alkaline phosphatase (IAP) is a brush-border phosphomonoesterase. Its location suggests an involvement in the uptake of nutrients, but its role has not yet been defined. IAP expression parallels that of other proteins involved in Ca absorption under vitamin D stimulation. Experiments carried out in vitro with purified IAP have demonstrated an interaction between Ca and IAP. The gut is prepared to face different levels of Ca intake over time, but high Ca intake in a situation of a low-Ca diet over time would cause excessive entry of Ca into the enterocytes. The presence of a mechanism to block Ca entry and to avoid possible adverse effects is thus predictable. Thus, in the present study, Sprague–Dawley rats were fed with different amounts of Ca in the diet (0·2, 1 and 2 g%), and the percentage of Ca absorption (%Ca) in the presence and absence of l-phenylalanine (Phe) was calculated. The presence of Phe caused a significant increase in %Ca (52·3 (sem 6·5) % in the presence of Phe v. 31·1 (sem 8·9) % in the absence of Phe, regardless of the amount of Ca intake; paired t test, P = 0·02). When data were analysed with respect to Ca intake, a significant difference was found only in the group with low Ca intake (paired t test, P = 0·03). Additionally, IAP activity increased significantly (ANOVA, P < 0·05) as Ca concentrations increased in the duodenal lumen. The present study provides in vivo evidence that luminal Ca concentration increases the activity of IAP and simultaneously decreases %Ca, acting as a minute-to-minute regulatory mechanism of Ca entry.

Regular consumption of fruit and vegetables may be associated with decreased CVD risk. In the present study, we investigated the effects of blackcurrant (BC) juice, rich in polyphenols and ascorbic acid, on oxidative and inflammatory biomarkers in cultured macrophages in vitro and in human subjects with an atherosclerosis-prone phenotype (after consumption of a high-energy meal). In cultured macrophages (RAW264.7), BC treatment significantly inhibited lipopolysaccharide-induced inflammation as indicated by lower mRNA levels of TNF-α, IL-1β and inducible NO synthase (iNOS) and lower nuclear p65 levels indicating decreased NF-κB activity. iNOS protein levels were lower and haem oxygenase 1 levels higher in BC-treated cells when compared with untreated controls. Subjects given a high-energy meal had elevated serum glucose and insulin levels with no significant difference between the BC-based juice and placebo treatment groups. TAG following meal ingestion tended to be attenuated after the BC treatment. Plasma ascorbic acid and radical-scavenging capacity were decreased following placebo meal consumption; however, BC significantly elevated both parameters compared with baseline and placebo ingestion. Plasma oxidised LDL, α-tocopherol and paraoxonase activity were unchanged in both treatment groups. Furthermore, production of TNF-α and IL-1β was not significantly changed by BC meal consumption. The present results suggest potential antioxidative and anti-inflammatory properties of BC in vitro in cultured macrophages. Although the observations were not directly transferable to a postprandial in vivo situation, the present results show that BC juice consumption may improve postprandial antioxidant status as indicated by higher ascorbic acid levels and free radical-scavenging capacity in plasma.

The development of lower-glycaemic index (GI) foods requires simple, palatable and healthy strategies. The objective of the present study was to determine the most effective dose of a novel viscous fibre supplement (PGX®) to be added to starchy foods to reduce their GI. Healthy subjects (n 10) consumed glucose sugar (50 g in water × 3) and six starchy foods with a range of GI values (52–72) along with 0 (inert fibre), 2·5 or 5 g granular PGX® dissolved in 250 ml water. GI testing according to ISO Standard 26 642-2010 was used to determine the reduction in GI. PGX® significantly reduced the GI of all six foods (P < 0·001), with an average reduction of 19 % for the 2·5 g dose and 30 % for the 5 g dose, equivalent to a reducing the GI by 7 and 15 units, respectively. Consuming small quantities of the novel functional fibre PGX®, mixed with water at the start of a meal, is an effective strategy to reduce the GI of common foods.

The aim of the present study was to investigate the effects of grape seed extract (GSE) supplementation on exercise performance and oxidative stress in acutely and chronically exercised rats. A total of sixty-four male rats were used in the study. Rats were divided into six groups: control, chronic exercise control, acute exercise control (AEC), GSE-supplemented control, GSE-supplemented chronic exercise and GSE-supplemented acute exercise groups. Chronic exercise consisted of treadmill running at 25 m/min, 45 min/d, 5 d a week for 6 weeks. Rats in the acute exercise groups were run on the treadmill at 30 m/min until exhaustion. GSE were given at 100 mg/kg of body weight with drinking water for 6 weeks. Plasma was separated from blood samples for the analysis of oxidative stress markers. There was no significant difference in time of exhaustion between the acute exercise groups. Plasma malondialdehyde (MDA) levels were higher in the acute exercise groups and lower in the chronic exercise groups. GSE supplementation decreased MDA levels. Xanthine oxidase and adenosine deaminase activities were higher in the AEC group compared to all the other groups. NO levels were increased with both chronic exercise and GSE supplementation. Superoxide dismutase and glutathione peroxidase activities were lower in the acute exercised groups and higher in the chronic exercised groups. GSE supplementation caused an increase in antioxidant enzyme activities. In conclusion, GSE supplementation prevents exercise-induced oxidative stress by preventing lipid peroxidation and increasing antioxidant enzyme activities.

The aim of the present study was to elucidate possible cholesterol-lowering mechanism(s) of high-dose supplemental Se in the form of selenite, a known hypocholesterolaemic agent. Male Syrian hamsters (four groups, ten per group) were fed semi-purified diets for 4 weeks containing 0·1 % cholesterol and 15 % saturated fat with selenite corresponding to varying levels of Se: (1) Se 0·15 parts per million (ppm), control diet; (2) Se 0·85 ppm; (3) Se 1·7 ppm; (4) Se 3·4 ppm. Lipids were measured in the bile, faeces, liver and plasma. The mRNA expression of several known regulators of cholesterol homeostasis (ATP-binding cassette transporters g5 (Abcg5) and g8 (Abcg8), 7-hydroxylase, 3-hydroxy-3-methylglutaryl-coenzyme A reductase, LDL receptor (LdLr) and Nieman-Pick C1-like 1 protein (Npc1l1)) were measured in the liver and/or jejunum. Oxysterols including 24-(S)-hydroxycholesterol, 25-hydroxycholesterol and 27-hydroxycholesterol (27-OHC) were measured in the liver. Significantly lower total plasma cholesterol concentrations were observed in hamsters consuming the low (0·85 ppm) and high (3·4 ppm) Se doses. The two highest doses of Se resulted in decreased plasma LDL-cholesterol concentrations and increased mRNA levels of hepatic Abcg8, Ldlr and jejunal Ldlr. Higher hepatic 27-OHC and TAG concentrations and lower levels of jejunal Npc1l1 mRNA expression were noted in the 1·7 and 3·4 ppm Se-treated hamsters. Overall, Se-induced tissue changes in mRNA expression including increased hepatic Abcg8 and Ldlr, increased jejunal Ldlr and decreased jejunal Npc1l1, provide further elucidation regarding the hypocholesterolaemic mechanisms of action of Se in the form of selenite.

In the present study, two experiments were conducted to investigate the effect of Mn source on Mn transport and the expression of a Mn transporter, divalent metal transporter 1 (DMT1), in the small intestine of broilers. In Expt 1, in situ ligated duodenal loops from Mn-deficient chicks (29-d-old) were perfused with solutions containing 0–8·74 mmol Mn/l from either MnSO4, or one of two organic chelates of Mn and amino acids with moderate (OM) or strong (OS) chelation strength (Qf) up to 30 min. In Expt 2, Mn-deficient intact broilers (14-d-old) were fed a control diet (12·45 mg Mn/kg) or the control diet supplemented with 100 mg Mn/kg as one of all Mn sources for 14 d. The uptake kinetics of Mn from different Mn sources in the ligated duodenal loops followed a saturable process as determined by regression analysis of concentration-dependent uptake rates. The maximum transport rate (Jmax) and Km values, and DMT1 mRNA levels in the ligated duodenal loops were higher (P < 0·01) for OM and OS than for MnSO4. DMT1 mRNA levels were much higher (P < 0·01) in the duodenum than in the jejunum and ileum. Both DMT1 mRNA levels in the duodenum and plasma Mn contents from the hepatic portal vein of intact chicks on day 14 post-feeding increased (P < 0·05) in the following order: control < MnSO4 < OM < OS. These results indicated that organic Mn sources with stronger Qf showed higher Mn transport and absorption, and DMT1 might be involved in the regulation of organic Mn transport in the proximal small intestine of broilers.

The effect of the type of non-protein energy (NPE) on energy utilisation in Nile tilapia was studied, focusing on digestible energy utilisation for growth (kgDE). Furthermore, literature data on kgDE across fish species were analysed in order to evaluate the effect of dietary macronutrient composition. A total of twelve groups of fish were assigned in a 2 × 2 factorial design: two diets (‘fat’ v. ‘starch’) and two feeding levels (‘low’ v. ‘high’). In the ‘fat’-diet, 125 g fish oil and in the ‘starch’-diet 300 g maize starch were added to 875 g of an identical basal mixture. Fish were fed restrictively one of two ration levels (‘low’ or ‘high’) for estimating kgDE. Nutrient digestibility, N and energy balances were measured. For estimating kgDE, data of the present study were combined with previous data of Nile tilapia fed similar diets to satiation. The type of NPE affected kgDE (0·561 and 0·663 with the ‘starch’ and ‘fat’-diets, respectively; P < 0·001). Across fish species, literature values of kgDE range from 0·31 to 0·82. Variability in kgDE was related to dietary macronutrient composition, the trophic level of the fish species and the composition of growth (fat:protein gain ratio). The across-species comparison suggested that the relationships of kgDE with trophic level and with growth composition were predominantly induced by dietary macronutrient composition. Reported kgDE values increased linearly with increasing dietary fat content and decreasing dietary carbohydrate content. In contrast, kgDE related curvilinearly to dietary crude protein content. In conclusion, energy utilisation for growth is influenced by dietary macronutrient composition.

The non-extractable fraction of many fruit and vegetables contains putatively bioactive polyphenolic compounds that, in most cases, have not been well characterised structurally. Non-extractable proanthocyanidins (NEPA) of a polymeric nature are part of the dietary fibre fraction of food. Using liquid chromatography coupled to a mass spectrometer equipped with an electrospray ionisation chamber and a triple quadrupole mass analyser for tandem analysis (HPLC–ESI–QqQ–MS/MS) techniques, we examine the phenolic metabolites present in urine and faeces from rats 24 h after ingestion of an NEPA-rich fraction. We show that NEPA are partially depolymerised during their transit along the intestinal tract, as evidenced by the presence of (epi)catechin (EC) monomers and dimers in faeces and phase II conjugates of EC in urine. Moreover, NEPA are further metabolised by the intestinal microbiota into smaller metabolites including phenolic acids that are present in urine as both free phenolics and conjugates with glucuronate or sulphate moieties. For the first time, we report evidence that NEPA behave in vivo as a source of phenolics that are released progressively and deliver phenolic species that come into contact with the intestinal walls and are bioavailable for at least 24 h after ingestion.

It is well established that altered maternal nutrition may induce long-term metabolic consequences in offspring. However, the effects of maternal undernutrition during different developmental windows on sex-specific growth and metabolism in offspring are not well defined. We investigated the effect of moderate maternal undernutrition during pregnancy and/or lactation on postnatal growth and metabolic outcomes in offspring. Wistar rats were randomly assigned to one of four groups: (1) control (CONT) dams fed a standard diet throughout pregnancy and lactation; (2) dams undernourished to 50 % of CONT during pregnancy (UNP); (3) dams fed at 50 % of CONT throughout lactation (UNL); (4) dams fed at 50 % of CONT throughout pregnancy and lactation (UNPL). UNP and UNPL offspring were lighter at birth compared to CONT and UNL. UNL and UNPL offspring were growth restricted at weaning and remained smaller into adulthood. UNP males and females developed increased adiposity and hyperleptinaemia in adulthood compared to all other groups. Adiposity in UNL and UNPL males was similar to CONT offspring. In UNL and UNPL females, adiposity was lower than for CONT females. Markers of bone mass, lipid metabolism and hepatic function were altered in UNP offspring but were similar in UNL and UNPL offspring compared to CONT. Lack of catch-up growth during lactation in offspring of undernourished mothers prevented development of adiposity and related metabolic disorders in later life. These data highlight that the timing and duration of undernutrition during critical windows of development exert differential effects on postnatal outcomes in a sex-specific manner.

Dietary probiotics supplementation exerts beneficial health effects. Since cigarette smoking reduces natural killer (NK) activity, we evaluated the effect of Lactobacillus casei Shirota (LcS) intake on NK cytotoxic activity in male smokers. The double-blind, placebo-controlled, randomised study was conducted on seventy-two healthy Italian blue-collar male smokers randomly divided for daily intake of LcS powder or placebo. Before and after 3 weeks of intake, peripheral blood mononuclear cells were isolated and NK activity and CD16+ cells' number were assessed. Daily LcS intake for 3 weeks significantly increased NK activity (P < 0·001). The increase in NK activity was paralleled by an increase in CD16+ cells (P < 0·001). Before intake, NK cytotoxic activity inversely correlated with the number of cigarettes smoked (R − 0·064). LcS intake prevented the smoke-dependent expected NK activity reduction. The analysis of the distribution of changes in smoke-adjusted NK activity demonstrated that the positive variations were significantly associated with LcS intake, while the negative variations were associated with placebo intake (median value of distributions of differences, 20·98 lytic unit (LU)/107 cells for LcS v. − 4·38 LU/107 cells for placebo, P = 0·039). In conclusion, 3 weeks of daily LcS intake in Italian male smokers was associated with a higher increase in cytotoxic activity and CD16+ cells' number in comparison to the placebo intake group.

Intake of fish oil reduces the risk of CHD and CHD deaths. Marine n-3 fatty acids (FA) are susceptible to oxidation, but to our knowledge, the health effects of intake of oxidised fish oil have not previously been investigated in human subjects. The aim of the present study was to investigate markers of oxidative stress, lipid peroxidation and inflammation, and the level of plasma n-3 FA after intake of oxidised fish oil. In a double-blinded randomised controlled study, healthy subjects (aged 18–50 years, n 54) were assigned into one of three groups receiving capsules containing either 8 g/d of fish oil (1·6 g/d EPA+DHA; n 17), 8 g/d of oxidised fish oil (1·6 g/d EPA+DHA; n 18) or 8 g/d of high-oleic sunflower oil (n 19). Fasting blood and morning spot urine samples were collected at weeks 0, 3 and 7. No significant changes between the different groups were observed with regard to urinary 8-iso-PGF2α; plasma levels of 4-hydroxy-2-hexenal, 4-hydroxy-2-nonenal and α-tocopherol; serum high sensitive C-reactive protein; or activity of antioxidant enzymes in erythrocytes. A significant increase in plasma level of EPA+DHA was observed in both fish oil groups, but no significant difference was observed between the fish oil groups. No changes in a variety of in vivo markers of oxidative stress, lipid peroxidation or inflammation were observed after daily intake of oxidised fish oil for 3 or 7 weeks, indicating that intake of oxidised fish oil may not have unfavourable short-term effects in healthy human subjects.

PUFA from fish oil appear to have anti-inflammatory and anti-oxidative effects and improve nutritional status in cancer patients. With this as background, the aim of the present study was to investigate the effect of EPA plus DHA on inflammatory condition, and oxidative and nutritional status in patients with lung cancer. In our multicentre, randomised, double-blind trial, thirty-three patients with a diagnosis of advanced inoperable non-small-cell lung cancer and undergoing chemotherapy were divided into two groups, receiving four capsules/d containing 510 mg of EPA and 340 mg of DHA, or 850 mg of placebo, for 66 d. At the start of chemotherapy (T0), after 8 d (T1), 22 d (T2) and 66 d (T3), biochemical (inflammatory and oxidative status parameters) and anthropometric parameters were measured in both groups. A significant increase of body weight in the n-3 group at T3v. T0 was observed. Concerning inflammation, C-reactive protein and IL-6 levels differed significantly between the n-3 and placebo groups at T3, and progressively decreased during chemotherapy in the n-3 group, evidencing n-3 PUFA anti-inflammatory action. Concerning oxidative status, plasma reactive oxygen species levels increased in the placebo group v. the n-3 group at the later treatment times. Hydroxynonenal levels increased in the placebo group during the study, while they stabilised in the n-3 group. Our data confirm that the continual assumption of EPA plus DHA determined an anti-inflammatory and anti-oxidative action which could be considered a preliminary goal in anti-cachectic therapy.

The aim of the present study was to compare the effect of lutein- and zeaxanthin-rich foods and supplements on macular pigment level (MPL) and serological markers of endothelial activation, inflammation and oxidation in healthy volunteers. We conducted two 8-week intervention studies. Study 1 (n 52) subjects were randomised to receive either carrot juice (a carotene-rich food) or spinach powder (a lutein- and zeaxanthin-rich food) for 8 weeks. Study 2 subjects (n 75) received supplements containing lutein and zeaxanthin, β-carotene, or placebo for 8 weeks in a randomised, double-blind, placebo-controlled trial. MPL, serum concentrations of lipid-soluble antioxidants, inter-cellular adhesion molecule 1, vascular cell adhesion molecule 1, C-reactive protein and F2-isoprostane levels were assessed at baseline and post-intervention in both studies. In these intervention studies, no effects on MPL or markers of endothelial activation, inflammation or oxidation were observed. However, the change in serum lutein and zeaxanthin was associated or tended to be associated with the change in MPL in those receiving lutein- and zeaxanthin-rich foods (lutein r 0·40, P = 0·05; zeaxanthin r 0·30, P = 0·14) or the lutein and zeaxanthin supplement (lutein r 0·43, P = 0·03; zeaxanthin r 0·22, P = 0·28). In both studies, the change in MPL was associated with baseline MPL (food study r − 0·54, P < 0·001; supplement study r − 0·40, P < 0·001). We conclude that this 8-week supplementation with lutein and zeaxanthin, whether as foods or as supplements, had no significant effect on MPL or serological markers of endothelial activation, inflammation and oxidation in healthy volunteers, but may improve MPL in the highest serum responders and in those with initially low MPL.

In the present study, we aimed to validate the Malnutrition Universal Screening Tool (MUST) for routine nutritional screening in the radiation oncology setting, thus enabling timely and adequate referrals of patients at risk for individualised or advanced intervention. Towards this objective, we conducted a prospective cross-sectional study in 450 non-selected cancer patients (18–95 years) referred for radiotherapy. The following were the nutritional parameters: BMI (categorised by WHO's age/sex criteria), weight loss >5 % in the previous 3–6 months, Patient-Generated Subjective Global Assessment (PG-SGA – validated/specific for oncology) and nutritional risk by MUST. Sensitivity, specificity, predictive values and concordance were calculated to validate MUST v. PG-SGA and compare single parameters v. PG-SGA/MUST. BMI v. PG-SGA showed a negligible capacity to detect undernutrition: 0·27 sensitivity, 0·23 specificity, 0·35 positive predictive value and 0·31 negative predictive value. Conversely, percentage weight loss v. PG-SGA was highly effective: 0·76 sensitivity, 0·85 specificity, 0·79 positive predictive value and 0·85 negative predictive value. MUST v. PG-SGA successfully detected patients at risk: 0·80 sensitivity, 0·89 specificity, 0·87 positive predictive value and 1·0 negative predictive value; percentage weight loss v. MUST proved able to identify patients likely to be at risk: 0·85 sensitivity, 0·91 specificity, 0·90 positive predictive value and 1·0 negative predictive value. This is the first study in the radiation oncology setting to validate MUST: a simple and quick method applicable by any health professional, with a high validity for early screening, ideally to antedate a comprehensive nutritional assessment and guide for intervention. In this study, percentage weight loss in the previous 3–6 months does seem valid to predict nutritional risk, and may be the minimum in a busy routine.

The relationship between dietary intake and obesity is complex, and dietary pattern analysis may offer new insight. We examined associations between dietary patterns identified in a diverse cohort of adolescents and weight status cross-sectionally and over a 5-year period. Project EAT (Eating Among Teens) (Time 1) collected data on 4746 middle (younger cohort) and high school (older cohort) students in 1998–9. EAT-II (Time 2) resurveyed 2516 of the original cohort in 2003–4. All analyses were run separately by age cohort and sex. The relationship between dietary patterns identified previously (vegetable, fruit, vegetable & fruit, starchy food, sweet & salty snack food, and fast food) and weight status was examined using logistic regression. All analyses were adjusted for socioeconomic status, race/ethnicity and activity level (longitudinal analyses were also adjusted for baseline weight status). In cross-sectional analyses, higher adherence to dietary patterns loading heavily on vegetables was associated with lower risk of overweight/obese weight status in older and younger girls, whereas higher adherence to a ‘sweet & salty snack food’ pattern was associated with lower risk in older and younger boys. These associations were found prospectively in older boys and girls, but were no longer significant in analyses adjusting for baseline weight status. We did not find consistent or intuitive associations between dietary patterns and weight status. Identified patterns may not capture the elements of diet that are truly important in determining adolescent weight, or diet may not be the primary driver in determining weight status at this age. Methodological difficulties in assessing diet must also be taken into consideration.

In the present study, we investigated the prevalence of anaemia and Fe deficiency anaemia (IDA) and explored the relationship between Helicobacter pylori infection and IDA in adolescent girls. A total of 1037 adolescent girls from Suihua, China were enrolled. Hb, serum ferritin (SF), serum transferrin receptor (sTfR) and serum IgG antibodies to H. pylori were measured. Participants with IDA and co-existing H. pylori infection (n 80) who had an intake of >25 mg/d of Fe were assigned randomly to the intervention and control groups. Patients in the intervention group were administered a 12-week course of oral EDTA–Na–Fe (60 mg Fe/dose, three times a week) and a 2-week course of colloidal bismuth subcitrate, amoxicillin and metronidazole. Subjects in the control group were administered EDTA–Na–Fe alone. Hb, SF and sTfR were reassessed 3 months after the 12-week regimen ended. Prevalence of anaemia, Fe deficiency (defined as SF < 12·0 μg/l), IDA and H. pylori infection in the population of 1037 was 19·5, 40·4, 17·1 and 31·2 %, respectively. The prevalence of H. pylori infection in the IDA group was 46·9 %, while the non-anaemic group had 28·1 % prevalence. A significant increase in Hb and SF and a decrease in sTfR value were found in the intervention group and the H. pylori-negative group. Findings suggest that IDA is still one of the prominent problems in adolescent girls. There is an association between H. pylori infection and IDA. Treatment of H. pylori infection is associated with a more rapid response to oral Fe therapy.