In obese subjects, the loss of fat mass during energy restriction is often accompanied by a loss of muscle mass. The hypothesis that n-3 PUFA, which modulate protein homoeostasis via effects on insulin sensitivity, could contribute to maintain muscle mass during energy restriction was tested in rats fed a high-fat diet (4 weeks) rich in 18 : 1 n-9 (oleic acid, OLE-R), 18 : 3 n-3 (α-linolenic acid, ALA-R) or n-3 long-chain (LC-R) fatty acid and then energy restricted (8 weeks). A control group (OLE-ad libitum (AL)) was maintained with AL diet throughout the study. Rats were killed 10 min after an i.v. insulin injection. All energy-restricted rats lost weight and fat mass, but only the OLE-R group showed a significant muscle loss. The Gastrocnemius muscle was enriched with ALA in the ALA-R group and with LC-PUFA in the ALA-R and LC-R groups. The proteolytic ubiquitin–proteasome system was differentially affected by energy restriction, with MAFbx and muscle ring finger-1 mRNA levels being decreased in the LC-R group (−30 and −20 %, respectively). RAC-α serine/threonine-protein kinase and insulin receptor substrate 1 phosphorylation levels increased in the LC-R group (+70 %), together with insulin receptor mRNA (+50 %). The ALA-R group showed the same overall activation pattern as the LC-R group, although to a lesser extent. In conclusion, dietary n-3 PUFA prevent the loss of muscle mass associated with energy restriction, probably by an improvement in the insulin-signalling pathway activation, in relation to enrichment of plasma membranes in n-3 LC-PUFA.

This study aimed to verify the effect of aerobic exercise performed in the fasted v. fed states on fat and carbohydrate metabolism in adults. Searches were conducted in March 2015, and updated in July 2016, using PubMed®, Scopus and Cochrane databases (terms: ‘fasting’, ‘exercise’, ‘aerobic exercise’, ‘substrate’, ‘energy metabolism’, ‘fat’, ‘glucose’, ‘insulin’ and ‘adult’) and references from selected studies. Trials that compared the metabolic effects of aerobic exercise (duration ≤120 min) performed in the fasted v. fed states in adults were accepted. The outcomes evaluated were fat oxidation during exercise and the plasma concentrations of insulin, glucose and NEFA before and immediately after exercise; two independent reviewers extracted the data (A. F. V. and L. C.). The results were presented as weighted mean differences between treatments, with 95 % CI. Of 10 405 articles identified, twenty-seven studies – with a total of 273 participants – were included. There was a significant increase in fat oxidation during exercise performed in the fasted, compared with fed, state (−3·08 g; 95 % CI −5·38, −0·79; I2 39·1 %). The weighted mean difference of NEFA concentrations was not significantly different between states (0·00 mmol/l; 95 % CI −0·07, 0·08; I2 72·7 %). However, the weighted mean differences of glucose (0·78 mmol/l; 95 % CI 0·43, 1·14; I2 90·8 %) and insulin concentrations (104·5 pmol/l; 95 % CI 70·8, 138·2; I2 94·5 %) were significantly higher for exercise performed in the fed state. We conclude that aerobic exercise performed in the fasted state induces higher fat oxidation than exercise performed in the fed state.

The metabolic syndrome (MetS) is known to be associated with elevated serum ferritin levels. The possible association with other Fe markers has been less well studied. We aimed to investigate the cross-sectional association of soluble transferrin receptor (sTfR) and ferritin levels with the MetS components, insulin resistance and glycosylated Hb (HbA1C). The sample consisted of 725 adults, aged 19–93 years (284 men, 151 premenopausal and 290 postmenopausal women), from the Croatian island of Vis. Serum sTfR and ferritin levels were measured by immunoturbidimetry and electrochemiluminescence assays, respectively. The MetS was defined using modified international consensus criteria. Logistic and linear regression analyses were conducted to investigate the associations adjusting for age, fibrinogen, smoking status, alcohol consumption and BMI. Prevalence of the MetS was 48·7 %. Standardised values of ferritin were positively associated with all of the MetS components (except high blood pressure and waist circumference) in men (P<0·05). Ferritin was significantly associated with the MetS in men (adjusted OR 1·78 (95 % CI 1·31, 2·42)) and postmenopausal women (1·71 (95 % CI 1·12, 2·62)). Interestingly, sTfR was independently and positively associated with homoeostatic model assessment for insulin resistance in men (adjusted β=0·44 (95 % CI 0·14, 0·75), P=0·004) and postmenopausal women (adjusted β coefficient=0·34 (95 % CI 0·05, 0·63), P=0·020). However, there was no significant relationship between serum sTfR levels and the MetS or its components. Neither ferritin nor sTfR was significantly associated with HbA1C (P>0·05). sTfR levels could be spuriously elevated in subjects with insulin resistance and without association with the MetS or its components. We conclude that different markers of Fe metabolism are not consistently associated with cardiometabolic risk.

Necrotising enterocolitis (NEC) is a common disease in premature infants characterised by intestinal ischaemia and necrosis. The only effective preventative strategy against NEC is the administration of breast milk, although the protective mechanisms remain unknown. We hypothesise that an abundant human milk oligosaccharide (HMO) in breast milk, 2′-fucosyllactose (2′FL), protects against NEC by enhancing intestinal mucosal blood flow, and we sought to determine the mechanisms underlying this protection. Administration of HMO-2′FL protected against NEC in neonatal wild-type mice, resulted in a decrease in pro-inflammatory markers and preserved the small intestinal mucosal architecture. These protective effects occurred via restoration of intestinal perfusion through up-regulation of the vasodilatory molecule endothelial nitric oxide synthase (eNOS), as administration of HMO-2′FL to eNOS-deficient mice or to mice that received eNOS inhibitors did not protect against NEC, and by 16S analysis HMO-2′FL affected the microbiota of the neonatal mouse gut, although these changes do not seem to be the primary mechanism of protection. Induction of eNOS by HMO-2′FL was also observed in cultured endothelial cells, providing a link between eNOS and HMO in the endothelium. These data demonstrate that HMO-2′FL protects against NEC in part through maintaining mesenteric perfusion via increased eNOS expression, and suggest that the 2′FL found in human milk may be mediating some of the protective benefits of breast milk in the clinical setting against NEC.

Pro-inflammatory cytokines are critical in mechanisms of muscle atrophy. In addition, asparagine (Asn) is necessary for protein synthesis in mammalian cells. We hypothesised that Asn could attenuate lipopolysaccharide (LPS)-induced muscle atrophy in a piglet model. Piglets were allotted to four treatments (non-challenged control, LPS-challenged control, LPS+0·5 % Asn and LPS+1·0 % Asn). On day 21, the piglets were injected with LPS or saline. At 4 h post injection, piglet blood and muscle samples were collected. Asn increased protein and RNA content in muscles, and decreased mRNA expression of muscle atrophy F-box (MAFbx) and muscle RING finger 1 (MuRF1). However, Asn had no effect on the protein abundance of MAFbx and MuRF1. In addition, Asn decreased muscle AMP-activated protein kinase (AMPK) α phosphorylation, but increased muscle protein kinase B (Akt) and Forkhead Box O (FOXO) 1 phosphorylation. Moreover, Asn decreased the concentrations of TNF-α, cortisol and glucagon in plasma, and TNF-α mRNA expression in muscles. Finally, Asn decreased mRNA abundance of muscle toll-like receptor (TLR) 4 and nucleotide-binding oligomerisation domain protein (NOD) signalling-related genes, and regulated their negative regulators. The beneficial effects of Asn on muscle atrophy may be associated with the following: (1) inhibiting muscle protein degradation via activating Akt and inactivating AMPKα and FOXO1; and (2) decreasing the expression of muscle pro-inflammatory cytokines via inhibiting TLR4 and NOD signalling pathways by modulation of their negative regulators.

Partially hydrolysed guar gum (PHGG), a water-soluble dietary fibre produced by the controlled partial enzymatic hydrolysis of guar gum beans, has various physiological roles. This study aimed to elucidate the beneficial effects of PHGG on colonic mucosal damage in a murine 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis model. Acute colitis was induced in male C57BL/6 mice with TNBS after 2 weeks of pre-feeding with PHGG (5 %). The colonic mucosal inflammation was evaluated using macroscopic damage scores, and neutrophil infiltration was assessed by measuring tissue-associated myeloperoxidase (MPO) activity in the colonic mucosa. TNF-α expression in the colonic mucosa was measured by ELISA and real-time PCR. Moreover, the intestinal microbiota and production of SCFA were assessed by real-time PCR and HPLC, respectively. Colonic damage due to TNBS administration was significantly ameliorated by PHGG treatment. Furthermore, PHGG significantly inhibited increases in MPO activity and TNF-α protein and mRNA expression in the colonic mucosa in TNBS-induced colitis. On analysis of intestinal microbiota, we found that the concentration of the Clostridium coccoides group (Clostridium cluster XIVa), the Clostridium leptum subgroup (Clostridium cluster IV) and the Bacteroides fragilis group had significantly increased in PHGG-fed mice. On analysis of SCFA, we found that the caecal content of acetic acid, propionic acid and butyric acid had significantly increased in PHGG-fed mice. Together, these results suggest that chronic ingestion of PHGG prevents the development of TNBS-induced colitis in mice by modulating the intestinal microbiota and SCFA, which may be significant in the development of therapeutics for inflammatory bowel disease.

High fruit and vegetable (FAV) intake is associated with a lower prevalence of chronic diseases. Identifying the ideal number of FAV servings needed to reduce chronic disease risk is, however, difficult because of biases inherent to common self-report dietary assessment tools. The aim of our study was to examine the associations between daily FAV intake and plasma carotenoid concentrations in men and women enrolled in a series of fully controlled dietary interventions. We compiled and analysed data from a group of 155 men and 109 women who participated in six fully controlled dietary interventions and compared post-intervention fasting plasma carotenoid (α-carotene, β-carotene, β-cryptoxanthin, lutein, lycopene, zeaxanthin) concentrations with regard to the daily FAV servings consumed by the participants. We found that plasma β-cryptoxanthin, lutein and zeaxanthin concentrations were positively associated with daily FAV servings (P≤0·005). However, daily FAV intake was negatively associated with plasma α-carotene (P<0·0005) and lycopene (P<0·0001) concentrations, whereas no association was noted with plasma β-carotene. When men and women were analysed separately, we found that for any given number of FAV servings consumed women had higher circulating lutein concentrations compared with men (P<0·01). Significant sex×FAV (P<0·0001) and sex×dietary β-cryptoxanthin (P<0·0005) interactions were also noted favouring higher plasma β-cryptoxanthin concentrations in women than in men for a given FAV consumption. Results from these fully controlled dietary feeding studies indicate that plasma β-cryptoxanthin and lutein concentrations can be used as robust biomarkers of FAV consumption. They also suggest the existence of sex differences influencing circulating β-cryptoxanthin and lutein concentrations following FAV consumption.

Apart from the well-known action of insulin, the mechanism by which soya and cows’ milk improve postprandial glycaemia control was examined. In total, twelve healthy, young, Chinese men were studied on three separate occasions, in random order with isovolumetric (322 ml) control water, soya milk and cows’ milk. Plasma total amino acid concentrations increased 30 min after test meals consumption and were higher after soya milk (230 %) and cow milk (240 %) consumption compared with water. Cows’ milk ingestion induced higher branched-chain amino acids (BCAA) (40 %) than soya milk. Postprandial incretin concentrations increased after meal consumption. Cows’ milk meal was accompanied by higher incremental AUC (iAUC) (170 %) for glucagon-like peptide-1 (GLP-1) compared with soya milk and control (P=0·06). However, glucose-dependent insulinotropic polypeptide (GIP) concentrations increased to significantly greater levels after soya milk consumption (iAUC 60 % higher) compared with cows’ milk and control. Consumption of both soya and cows’ milk with carbohydrates induced a similar reduction in glycaemic response through a different mechanism, beyond insulin action. Plasma amino acids (alanine and arginine), and incretins in particular (GIP was stimulated), may be involved in the hyperinsulinaemia after soya milk meals. However, BCAA and GLP-1 release may be responsible for the reduced glycaemia after cows’ milk consumption by delaying gastric emptying. This could be the result of different milk protein/amino acid composition, but also differences in milk carbohydrate composition (i.e. lactose v. sucrose). It can be concluded that soya milk is a good alternative to cows’ milk with regard to glycaemic regulation, with different mechanisms involved.

This study was carried out to assess the effects of Se supplementation on biomarkers of inflammation and oxidative stress in patients with diabetic nephropathy (DN). This randomised, double-blind, placebo-controlled clinical trial was conducted among sixty patients with DN. Patients were randomly divided into two groups to take either 200 µg/d Se supplements as Se yeast (n 30) or placebo (n 30) for 12 weeks. In unadjusted analyses, compared with the placebo, Se supplementation led to a significant reduction in high-sensitivity C-reactive protein (hs-CRP) (−1069·2 (sd 1752·2) v. −135·3 (sd 1258·9) ng/ml, P=0·02), matrix metalloproteinase-2 (MMP-2) (−612·3 (sd 679·6) v. +76·0 (sd 309·1) ng/ml, P<0·001) and plasma malondialdehyde (MDA) concentrations (−0·1 (sd 0·7) v. +0·4 (sd 0·9) µmol/l, P=0·01). In addition, a significant increase in plasma total antioxidant capacity (TAC) (+174·9 (sd 203·9) v. +15·8 (sd 382·2) mmol/l, P=0·04) was observed following supplementation with Se compared with the placebo. Subjects who received Se supplements experienced a borderline statistically significant decrease in serum protein carbonyl (PCO) levels (P=0·06) compared with the placebo. When we adjusted the analysis for baseline values of biochemical parameters, age and BMI, serum hs-CRP (P=0·14) and MDA levels (P=0·16) became non-significant, whereas plasma nitric oxide (NO) (P=0·04) and glutathione (GSH) (P<0·001) became statistically significant, and other findings did not change. Supplementation with Se had no significant effect on NO, transforming growth factor β (TGF-β), advanced glycation end products (AGE), PCO and GSH compared with the placebo. Overall, our study demonstrated that Se supplementation among DN patients had favourable effects on serum MMP-2, plasma NO, TAC and GSH, but did not affect hs-CRP, TGF-β, AGE, PCO and MDA.

It has been previously shown that Lactobacillus plantarum CRL 2130 is able to produce riboflavin in soyamilk. The aim of the present study was to evaluate the efficiency of this riboflavin-bio-enriched soyamilk to revert and/or prevent the nutritional deficiency of riboflavin using different animal models. When used to supplement the diets of previously depleted animals, it was shown that the growth, riboflavin status and morphology of the small intestines reverted to normal parameters and were similar to animals supplemented with commercial riboflavin. In the prevention model, the same tendency was observed, where animals that received soyamilk fermented with L. plantarum CRL 2130 did not show signs of riboflavin deficiency. This new bio-fortified soya-based product could be used as part of normal diets to provide a more natural alternative to mandatory fortification with riboflavin for the prevention of its deficiency.

To examine the prevalence of folate inadequacy and toxicity based on usual intakes from food and supplements, as well as biomarkers of folate, secondary data analyses were performed using cross-sectional, nationally representative data from the Canadian Community Health Survey, Cycle 2.2 (n 32 776), as well as biomarker data from the Canadian Health Measures Survey, Cycles 1, 2 and 3 (n 15 754). On the basis of unfortified food sources, Canadians would struggle to consume adequate amounts of folate. When folate intakes from all food sources were considered, the overall prevalence of folate inadequacy was low across all age/sex groups, with the exception of females >70 years. However, >10 % of supplement users were above the tolerable upper intake level, increasing to almost 18 % when overage factors were accounted for. In addition, between 20 and 52 % of supplement users had elevated erythrocyte folate concentrations, depending on the cut-off used. Results from this study suggest that insufficient dietary intakes of folate in Canadians have been ameliorated because of the fortification policy, although folate inadequacy still exists across all age groups. However, supplement users appear to be at an increased risk of folic acid (FA) overconsumption as well as elevated erythrocyte folate. As such, the general population should be informed of the potential risks of FA overconsumption resulting from supplement use. This study suggests a need for more careful assessment of the risks and benefits of food fortification, particularly fortification above mandated levels, and FA supplement use in the general population.

Dietary patterns are a major risk factor for cardiovascular morbidity and mortality; however, few studies have examined this relationship in older adults. We examined prospective associations between dietary patterns and the risk of CVD and all-cause mortality in 3226 older British men, aged 60–79 years and free from CVD at baseline, from the British Regional Heart Study. Baseline FFQ data were used to generate thirty-four food groups. Principal component analysis identified dietary patterns that were categorised into quartiles, with higher quartiles representing higher adherence to the dietary pattern. Cox proportional hazards examined associations between dietary patterns and risk of all-cause mortality and cardiovascular outcomes. We identified three interpretable dietary patterns: ‘high fat/low fibre’ (high in red meat, meat products, white bread, fried potato, eggs), ‘prudent’ (high in poultry, fish, fruits, vegetables, legumes, pasta, rice, wholemeal bread, eggs, olive oil) and ‘high sugar’ (high in biscuits, puddings, chocolates, sweets, sweet spreads, breakfast cereals). During 11 years of follow-up, 899 deaths, 316 CVD-related deaths, 569 CVD events and 301 CHD events occurred. The ‘high-fat/low-fibre’ dietary pattern was associated with an increased risk of all-cause mortality only, after adjustment for confounders (highest v. lowest quartile; hazard ratio 1·44; 95 % CI 1·13, 1·84). Adherence to a ‘high-sugar’ diet was associated with a borderline significant trend for an increased risk of CVD and CHD events. The ‘prudent’ diet did not show a significant trend with cardiovascular outcomes or mortality. Avoiding ‘high-fat/low-fibre’ and ‘high-sugar’ dietary components may reduce the risk of cardiovascular events and all-cause mortality in older adults.

Exposures to antioxidants (AO) are associated with levels of C-reactive protein (CRP), but the pattern of evidence is mixed, due in part to studying each potential AO, one at a time, when multiple AO exposures might affect CRP levels. By studying multiple AO via a composite indicator approach, we estimate the degree to which serum CRP level is associated with serum AO level. Standardised field survey protocols for the US National Health and Nutrition Examination Survey (NHANES) 2003–2006 yielded nationally representative cross-sectional samples of adults aged 20 years and older (n 8841). NHANES latex-enhanced nephelometry quantified serum CRP levels. Liquid chromatography quantified serum concentrations of vitamins A, E and C and carotenoids. Using structural equations, we regressed CRP level on AO levels, and derived a summary estimate for a composite of these potential antioxidants (CPA), with covariates held constant. The association linking CPA with CRP was inverse, stronger for slightly elevated CRP (1·8≤CRP<10 mg/l; slope= −1·08; 95 % CI −1·39, −0·77) and weaker for highly elevated CRP (≥10 mg/l; slope= −0·52; 95 % CI −0·68, −0·35), with little change when covariates were added. Vitamins A and C, as well as lutein+zeaxanthin, were prominent contributors to the composite. In these cross-sectional data studied via a composite indicator approach, the CPA level and the CRP level were inversely related. The stage is set for more confirmatory longitudinal or intervention research on multiple vitamins. The composite indicator approach might be most useful in epidemiology when several exposure constructs are too weakly inter-correlated to be studied via formal measurement models for underlying latent dimensions.

This study explored associations between free sugars intake (using non-milk extrinsic sugars as proxy) and nutrient intakes among children aged 1·5–18 years in the UK National Diet and Nutrition Survey 2008–2012. Dietary records were completed by 2073 children (95 % completed 4 d). Mean free sugars intakes (% energy) were 11·8, 14·7 and 15·4 % in the 1·5–3, 4–10 and 11–18 years age groups, respectively. Nutrient intakes and nutrient density were compared across quintiles (Q1–Q5) of free sugars intake (% energy) within each age group. Energy intake rose from Q1 to Q5 of free sugars, whereas percentages of energy intake from fat, SFA and protein dropped. Associations with micronutrients (mg/d or mcg/d) were mostly non-significant, but among 11–18-year-olds there were significant negative associations with Zn, Se, Fe, Cu, and vitamin A and D. There were stronger negative associations with micronutrient density (mg/mcg per 4·18 MJ) for most nutrients in all age groups. Associations with vitamin C were positive. Results were similar after excluding misreporters. Children aged 4–18 years who consumed average amounts of free sugars or above (>13 % energy or Q3–Q5) had lower diet quality than those consuming <10 % free sugars (Q1), but there were insufficient data to assess diets with 5 % free sugars. High consumers obtained a higher proportion of free sugars from soft drinks, fruit juice and sugar confectionery and less from breakfast cereals. Ultimately, nutrient intakes depend on the total dietary pattern; however, reducing overconsumption of sugary foods and drinks with low nutrient density may help improve diet quality.

Flavonoids may play an important role in the protective effects of vegetables, fruits and tea against colorectal cancer. However, associations between flavonoids and colorectal cancer risk are inconsistent, and a few studies have evaluated the effect of flavonoids from different dietary sources separately. This study aimed to evaluate associations of flavonoids intake from different dietary sources with colorectal cancer risk in a Chinese population. From July 2010 to December 2015, 1632 eligible colorectal cancer cases and 1632 frequency-matched controls (age and sex) completed in-person interviews. A validated FFQ was used to estimate dietary flavonoids intake. Multivariate logistical regression models were used to calculate the OR and 95 % CI of colorectal cancer risk after adjusting for various confounders. No significant association was found between total flavonoids and colorectal cancer risk, with an adjusted OR of 1·06 (95 % CI 0·85, 1·32) comparing the highest with the lowest quartile. Anthocyanidins, flavanones and flavones intakes from total diet were found to be inversely associated with colorectal cancer risk. Compared with the lowest quartile, the adjusted OR for the highest quartile were 0·80 (95 % CI 0·64, 1·00) for anthocyanidins, 0·28 (95 % CI 0·22, 0·36) for flavanones and 0·54 (95 % CI 0·43, 0·67) for flavones. All subclasses of flavonoids from vegetables and fruits were inversely associated with colorectal cancer. However, no significant association was found between tea flavonoids and colorectal cancer risk. These data indicate that specific flavonoids, specifically flavonoids from vegetables and fruits, may be linked with the reduced risk of colorectal cancer.

Socio-economic inequalities in childhood can determine dietary patterns, and therefore future health. This study aimed to explore associations between social vulnerabilities and dietary patterns assessed at two time points, and to investigate the association between accumulation of vulnerabilities and dietary patterns. A total of 9301 children aged 2–9 years participated at baseline and 2-year follow-up examinations of the Identification and prevention of Dietary- and lifestyle-induced health EFfects In Children and infantS study. In all, three dietary patterns were identified at baseline and follow-up by applying the K-means clustering algorithm based on a higher frequency of consumption of snacks and fast food (processed), sweet foods and drinks (sweet), and fruits and vegetables (healthy). Vulnerable groups were defined at baseline as follows: children whose parents lacked a social network, children from single-parent families, children of migrant origin and children with unemployed parents. Multinomial mixed models were used to assess the associations between social vulnerabilities and children’s dietary patterns at baseline and follow-up. Children whose parents lacked a social network (OR 1·31; 99 % CI 1·01, 1·70) and migrants (OR 1·45; 99 % CI 1·15, 1·83) were more likely to be in the processed cluster at baseline and follow-up. Children whose parents were homemakers (OR 0·74; 99 % CI 0·60, 0·92) were less likely to be in the processed cluster at baseline. A higher number of vulnerabilities was associated with a higher probability of children being in the processed cluster (OR 1·78; 99 % CI 1·21, 2·62). Therefore, special attention should be paid to children of vulnerable groups as they present unhealthier dietary patterns.

Studies about effects of school lunch on children’s cognition are rare; two previous studies (CogniDo, CogniDo PLUS) generally found no negative effects of lunch on children’s cognitive performance at the end of lunch break (i.e. 45 min after finishing lunch), but suggested potential beneficial effects for single parameters. Therefore, the present study investigated the hypothesis of potential positive effects of school lunch on cognitive performance at early afternoon (90 min after finishing lunch). A randomised, cross-over intervention trial was conducted at a comprehensive school with fifth and sixth grade students. Participants were randomised into two groups: On day 1, group 1 did not eat lunch, whereas group 2 received lunch ad libitum. On day 2 (1 week later), group 2 did not eat lunch and group 1 received lunch ad libitum. The cognitive parameters task switching, working memory updating and alertness were tested using a computerised test battery 90 min after finishing the meal. Of the 204 recruited children, fifty were excluded because of deviations from the study protocol or absence on one of the 2 test days, which resulted in 154 participants. Data showed no significant effects of lunch on task switching, working memory updating and alertness (P values between 0·07 and 0·79). The present study suggests that school lunch does not seem to have beneficial effects on children’s cognitive functions regarding the conducted tests at early afternoon. Together with our previous studies, we conclude that school lunch in general has no negative effects on cognitive performance in children. However, beneficial effects seem to be restricted to a relatively short time period after eating lunch.

Assessing energy requirements is a fundamental activity in clinical dietetic practice. The aim of this study was to investigate which resting energy expenditure (REE) predictive equations are the best alternatives to indirect calorimetry before and after an interdisciplinary therapy in Brazilian obese women. In all, twelve equations based on weight, height, sex, age, fat-free mass and fat mass were tested. REE was measured by indirect calorimetry. The interdisciplinary therapy consisted of nutritional, physical exercise, psychological and physiotherapy support during the course of 1 year. The average differences between measured and predicted REE, as well as the accuracy at the ±10 % level, were evaluated. Statistical analysis included paired t tests, intraclass correlation coefficients and Bland–Altman plots. Validation was based on forty obese women (BMI 30–39·9 kg/m2). Our major findings demonstrated a wide variation in the accuracy of REE predictive equations before and after weight loss in non-morbid, obese women. The equations reported by Harris–Benedict and FAO/WHO/United Nations University (UNU) were the only ones that did not show significant differences compared with indirect calorimetry and presented a bias <5 %. The Harris–Benedict equation provided 40 and 47·5 % accurate predictions before and after therapy, respectively. The FAO equation provided 35 and 47·5 % accurate predictions. However, the Bland–Altman analysis did not show good agreement between these equations and indirect calorimetry. Therefore, the Harris–Benedict and FAO/WHO/UNU equations should be used with caution for obese women. The need to critically re-assess REE data and generate regional and more homogeneous REE databases for the target population is reinforced.