Circulating vitamin C and carotenoids are used as biomarkers of fruit and vegetable intake in research, but their comparative validity has never been meta-analysed. PubMed, EMBASE, CENTRAL, CINAHL and Web of Science were systematically searched up to December 2013 for randomised trials of different amounts of fruit and vegetable provision on changes in blood concentrations of carotenoids or vitamin C. Reporting followed PRISMA guidelines. Evidence quality was assessed using the GRADE system. Random effects meta-analysis combined estimates and meta-regression tested for sub-group differences. In all, nineteen fruit and vegetable trials (n 1382) measured at least one biomarker, of which nine (n 667) included five common carotenoids and vitamin C. Evidence quality was low and between-trial heterogeneity (I2) ranged from 74 % for vitamin C to 94 % for α-carotene. Groups provided with more fruit and vegetables had increased blood concentrations of vitamin C, α-carotene, β-carotene, β-cryptoxanthin and lutein but not lycopene. However, no clear dose–response effect was observed. Vitamin C showed the largest between-group difference in standardised mean change from the pre-intervention to the post-intervention period (smd 0·94; 95 % CI 0·66, 1·22), followed by lutein (smd 0·70; 95 % CI 0·37, 1·03) and α-carotene (smd 0·63; 95 % CI 0·25, 1·01), but all CI were overlapping, suggesting that none of the biomarkers responded more than the others. Therefore, until further evidence identifies a particular biomarker to be superior, group-level compliance to fruit and vegetable interventions can be indicated equally well by vitamin C or a range of carotenoids. High heterogeneity and a lack of dose–response suggest that individual-level biomarker responses to fruit and vegetables are highly variable.

Epidemiological studies show that diet is linked to the risk of developing CVD. The objective of this meta-analysis was to estimate the association between empirically derived dietary patterns and CVD. PubMed was searched for observational studies of data-driven dietary patterns that reported outcomes of cardiovascular events. The association between dietary patterns and CVD was estimated using a random-effects meta-analysis with 95 % CI. Totally, twenty-two observational studies met the inclusion criteria. The pooled relative risk (RR) for CVD, CHD and stroke in a comparison of the highest to the lowest category of prudent/healthy dietary patterns in cohort studies was 0·69 (95 % CI 0·60, 0·78; I2=0 %), 0·83 (95 % CI 0·75, 0·92; I2=44·6 %) and 0·86 (95 % CI 0·74, 1·01; I2=59·5 %), respectively. The pooled RR of CHD in a case–control comparison of the highest to the lowest category of prudent/healthy dietary patterns was 0·71 (95 % CI 0·63, 0·80; I2=0 %). The pooled RR for CVD, CHD and stroke in a comparison of the highest to the lowest category of western dietary patterns in cohort studies was 1·14 (95 % CI 0·92, 1·42; I2=56·9 %), 1·03 (95 % CI 0·90, 1·17; I2=59·4 %) and 1·05 (95 % CI 0·91, 1·22; I2=27·6 %), respectively; in case–control studies, there was evidence of increased CHD risk. Our results support the evidence of the prudent/healthy pattern as a protective factor for CVD.

This systematic review aimed to assess the determinants of the parathyroid hormone (PTH) level response to vitamin D supplementation. We searched Medline, Google Scholar and the reference lists of previous reviews. All randomised controlled trials (RCT) on vitamin D supplementation that involved apparently healthy human subjects with a report of PTH were selected. Potential studies were screened independently and in duplicate. Results are summarised as mean differences with 95 % confidence intervals. Quality assessment, subgroup analysis, meta-analysis and meta-regression analysis were carried out. Thirty-three vitamin D supplementation RCT were included. Vitamin D supplementation significantly raised circulating 25-hydroxyvitamin D (25(OH)D) with significant heterogeneity among studies with a pooled mean difference (PMD) of 15.5 ng/ml (test for heterogeneity: P<0·001 and I2=97·3 %). Vitamin D supplementation significantly reduced PTH level with PMD of −8·0 pg/ml, with significant heterogeneity ((test for heterogeneity: P<0·001) and the I2 value was 97·3 %). In the subgroup analyses, the optimum treatment effect for PTH was observed with Ca doses of 600–1200 mg/d (−22·48 pg/ml), after the duration of a >12-month trial (−18·36 pg/ml), with low baseline 25(OH)D concentration of <20 ng/ml (−16·70 pg/ml) and in those who were overweight and obese (−18·11 pg/ml). Despite the present meta-analysis being hindered by some limitations, it provided some interesting evidence, suggesting that suppression of PTH level needs higher vitamin D intake (75 μg/d) than the current recommendations and longer durations (12 months), which should be taken into account for nutritional recommendations.

This study aimed to investigate the effects of daily intake of vitamin D-fortified yogurt drink (doogh) on central obesity indicators in subjects with type 2 diabetes (T2D) and the possible modulation of this effect by vitamin D receptor (VDR) Cdx-2 genotypes. A total of sixty T2D subjects were randomly allocated to two groups to receive either plain doogh (PD; n 29, containing 170 mg Ca and no vitamin D/250 ml) or vitamin D3-fortified doogh (FD; n 31, containing 170 mg Ca and 12·5 μg/250 ml) twice a day for 12 weeks. 25-hydroxyvitamin D (25(OH)D), glycaemic as well as adiposity indicators were evaluated before and after the intervention. VDR-Cdx-2 genotypes in extended number of T2D subjects in the FD group (n 60) were determined as AA, GA and GG. After 12 weeks, in FD compared with PD, serum 25(OH)D increased (+35·4 v. −4·8 nmol/l; P<0·001) and mean changes of waist circumference (WC; −1·3 v. +1·6 cm; P=0·02), body fat mass (FM; −1·9 v. +0·60 %; P=0·008), truncal fat (TF; −1·1 v. 0·13 %; P=0·003) and visceral adipose tissue (−0·80 v. +0·37 AU; P<0·001) decreased significantly. Circulating 25(OH)D was raised only in the AA group (34·8 nmo/l in AA group v. −6·4 nmol/l in AG and −1·6 nmol/l in GG groups; P<0·001), which was accompanied by a significant decrease in changes of WC (P=0·004), FM% (P=0·01) and TF% (P<0·001) in the AA genotype. Daily intake of vitamin D-FD for 12 weeks improved the central obesity indices in T2D subjects, and the improvement was more pronounced in the carriers of the AA genotype of VDR-Cdx-2.

In our previous studies, veratric acid (VA) shows beneficial effect on hypertension and its associated dyslipidaemia. In continuation, this study was designed to investigate the effect of VA, one of the major benzoic acid derivatives from vegetables and fruits, on cardiovascular remodelling in hypertensive rats, primarily assessed by functional studies using Langendorff isolated heart system and organ bath system. Hypertension was induced in male albino Wistar rats by oral administration of Nω-nitro-l-arginine methyl ester hydrochloride (l-NAME) (40 mg/kg body weight (b.w.)) in drinking water for 4 weeks. VA was orally administered at a dose of 40 mg/kg b.w. l-NAME-treated rats showed impaired cardiac ventricular and vascular function, evaluated by Langendorff isolated heart system and organ bath studies, respectively; a significant increase in the lipid peroxidation products such as thiobarbituric acid-reactive substances and lipid hydroperoxides in aorta; and a significant decrease in the activities of superoxide dismutase, catalase, glutathione peroxidase and levels of GSH, vitamin C and vitamin E in aorta. Fibrotic remodelling of the aorta and heart were assessed by Masson’s Trichrome staining and Van Gieson’s staining, respectively. In addition, l-NAME rats showed increased heart fibronectin expression assessed by immunohistochemical analysis. VA supplementation throughout the experimental period significantly normalised cardiovascular function, oxidative stress, antioxidant status and fibrotic remodelling of tissues. These results of the present study conclude that VA acts as a protective agent against hypertension-associated cardiovascular remodelling.

Herein we hypothesise the positive effects of kojibiose (KJ), a prebiotic disaccharide, selected for reducing hepatic expression of inflammatory markers in vivo that could modulate the severity of saturated arachidic acid (ARa)-induced liver dysfunction in hyperglycaemic rats. Animals were fed daily (20 d) with ARa (0·3 mg) together or not with KJ (22 mg approximately 0·5 %, w/w diet). Glucose, total TAG and cholesterol contents and the phospholipid profile were determined in serum samples. Liver sections were collected for the expression (mRNA) of enzymes and innate biomarkers, and intrahepatic macrophage and T-cell populations were analysed by flow cytometry. ARa administration increased the proportion of liver to body weight that was associated with an increased (by 11 %) intrahepatic macrophage population. These effects were ameliorated when feeding with KJ, which also normalised the plasmatic levels of TAG and N-acyl-phosphatidylethenolamine in response to tissue damage. These results indicate that daily supplementation of KJ significantly improves the severity of ARa-induced hepatic alterations.

β-Hydroxy-β-methylbutyrate (HMB), a leucine metabolite, has long been supplemented as a Ca salt (Ca-HMB) to increase strength and performance gains with exercise and to reduce recovery time. Recently, the free acid form of HMB (HMB-FA) has become commercially available in capsule form (gelcap). The current study was conducted to compare the bioavailability of HMB using the two commercially available capsule forms of HMB-FA and Ca-HMB. We also compared the pharmacokinetics of each form when administered mixed in water. Ten human subjects (five male and five female) were studied in a randomised crossover design. There was no significant sex by treatment interaction for any of the pharmacokinetic parameters measured. HMB-FA administered in capsules was more efficient than Ca-HMB capsule at HMB delivery with a 37 % increase in plasma clearance rate (74·8 (sem 4·0) v. 54·5 (sem 3·2) ml/min, P<0·0001) and a 76 % increase in peak plasma HMB concentration (270·2 (sem 17·8) v. 153·9 (sem 17·9) μmol/l, P<0·006), which was reached in one-third the time (P<0·009). When HMB-FA and Ca-HMB were administered in water, the differences still favoured HMB-FA, albeit to a lesser degree. Plasma HMB with HMB-FA administered in water was greater during the early phase of absorption (up to 45 min postadministration, P<0·05); this resulted in increased AUC during the first 60 min after administration, when compared with Ca-HMB mixed in water (P<0·03). In conclusion, HMB-FA in capsule form improves clearance rate and availability of HMB compared with Ca-HMB in capsule form.

Protein malnutrition promotes hepatic steatosis, decreases insulin-like growth factor (IGF)-I production and retards growth. To identify new molecules involved in such changes, we conducted DNA microarray analysis on liver samples from rats fed an isoenergetic low-protein diet for 8 h. We identified the fibroblast growth factor 21 gene (Fgf21) as one of the most strongly up-regulated genes under conditions of acute protein malnutrition (P<0·05, false-discovery rate<0·001). In addition, amino acid deprivation increased Fgf21 mRNA levels in rat liver-derived RL-34 cells (P<0·01). These results suggested that amino acid limitation directly increases Fgf21 expression. FGF21 is a polypeptide hormone that regulates glucose and lipid metabolism. FGF21 also promotes a growth hormone-resistance state and suppresses IGF-I in transgenic mice. Therefore, to determine further whether Fgf21 up-regulation causes hepatic steatosis and growth retardation after IGF-I decrease in protein malnutrition, we fed an isoenergetic low-protein diet to Fgf21-knockout (KO) mice. Fgf21-KO did not rescue growth retardation and reduced plasma IGF-I concentration in these mice. Fgf21-KO mice showed greater epididymal white adipose tissue weight and increased hepatic TAG and cholesterol levels under protein malnutrition conditions (P<0·05). Overall, the results showed that protein deprivation directly increased Fgf21 expression. However, growth retardation and decreased IGF-I were not mediated by increased FGF21 expression in protein malnutrition. Furthermore, FGF21 up-regulation rather appears to have a protective effect against obesity and hepatic steatosis in protein-malnourished animals.

High Na and low K intakes have adverse effects on blood pressure, which increases the risk for CVD. The role of endothelial dysfunction and inflammation in this pathophysiological process is not yet clear. In a randomised placebo-controlled cross-over study in untreated (pre)hypertensives, we examined the effects of Na and K supplementation on endothelial function and inflammation. During the study period, subjects were provided with a diet that contained 2·4 g/d of Na and 2·3 g/d of K for a 10 460 kJ (2500 kcal) intake. After 1-week run-in, subjects received capsules with supplemental Na (3·0 g/d), supplemental K (2·8 g/d) or placebo, for 4 weeks each, in random order. After each intervention, circulating biomarkers of endothelial function and inflammation were measured. Brachial artery flow-mediated dilation (FMD) and skin microvascular vasomotion were assessed in sub-groups of twenty-two to twenty-four subjects. Of thirty-seven randomised subjects, thirty-six completed the study. Following Na supplementation, serum endothelin-1 was increased by 0·24 pg/ml (95 % CI 0·03, 0·45), but no change was seen in other endothelial or inflammatory biomarkers. FMD and microvascular vasomotion were unaffected by Na supplementation. K supplementation reduced IL-8 levels by 0·28 pg/ml (95 % CI 0·03, 0·53), without affecting other circulating biomarkers. FMD was 1·16 % (95 % CI 0·37, 1·96) higher after K supplementation than after placebo. Microvascular vasomotion was unaffected. In conclusion, a 4-week increase in Na intake increased endothelin-1, but had no effect on other endothelial or inflammatory markers. Increased K intake had a beneficial effect on FMD and possibly IL-8, without affecting other circulating endothelial or inflammatory biomarkers.

Single doses of resveratrol have previously been shown to increase cerebral blood flow (CBF) with no clear effect on cognitive function or mood in healthy adults. Chronic resveratrol consumption may increase the poor bioavailability of resveratrol or otherwise potentiate its psychological effects. In this randomised, double-blind, placebo-controlled, parallel-groups study, a total of sixty adults aged between 18 and 30 years received either placebo or resveratrol for 28 d. On the 1st and 28th day of treatment, the performance of cognitively demanding tasks (serial subtractions, rapid visual information processing and 3-Back) (n 41 complete data sets) was assessed, alongside blood pressure (n 26) and acute (near-IR spectroscopy (NIRS)) and chronic (transcranial Doppler) measures of CBF (n 46). Subjective mood, sleep quality and health questionnaires were completed at weekly intervals (n 53/54). The results showed that the cognitive effects of resveratrol on day 1 were restricted to more accurate but slower serial subtraction task performance. The only cognitive finding on day 28 was a beneficial effect of resveratrol on the accuracy of the 3-Back task before treatment consumption. Subjective ratings of ‘fatigue’ were significantly lower across the entire 28 d in the resveratrol condition. Resveratrol also resulted in modulation of CBF parameters on day 1, as assessed by NIRS, and significantly increased diastolic blood pressure on day 28. Levels of resveratrol metabolites were significantly higher both before and after the day’s treatment on day 28, in comparison with day 1. These results confirm the acute CBF effects of resveratrol and the lack of interpretable cognitive effects.

Despite appropriate antiepileptic drug treatment, approximately one-third of humans and dogs with epilepsy continue experiencing seizures, emphasising the importance for new treatment strategies to improve the quality of life of people or dogs with epilepsy. A 6-month prospective, randomised, double-blinded, placebo-controlled cross-over dietary trial was designed to compare a ketogenic medium-chain TAG diet (MCTD) with a standardised placebo diet in chronically antiepileptic drug-treated dogs with idiopathic epilepsy. Dogs were fed either MCTD or placebo diet for 3 months followed by a subsequent respective switch of diet for a further 3 months. Seizure frequency, clinical and laboratory data were collected and evaluated for twenty-one dogs completing the study. Seizure frequency was significantly lower when dogs were fed the MCTD (2·31/month, 0–9·89/month) in comparison with the placebo diet (2·67/month, 0·33–22·92/month, P=0·020); three dogs achieved seizure freedom, seven additional dogs had ≥50 % reduction in seizure frequency, five had an overall <50 % reduction in seizures (38·87 %, 35·68–43·27 %) and six showed no response. Seizure day frequency were also significantly lower when dogs were fed the MCTD (1·63/month, 0–7·58/month) in comparison with the placebo diet (1·69/month, 0·33–13·82/month, P=0·022). Consumption of the MCTD also resulted in significant elevation of blood β-hydroxybutyrate concentrations in comparison with placebo diet (0·041 (sd 0·004) v. 0·031 (sd 0·016) mmol/l, P=0·028). There were no significant changes in serum concentrations of glucose (P=0·903), phenobarbital (P=0·422), potassium bromide (P=0·404) and weight (P=0·300) between diet groups. In conclusion, the data show antiepileptic properties associated with ketogenic diets and provide evidence for the efficacy of the MCTD used in this study as a therapeutic option for epilepsy treatment.

The aim of the present study was to examine the associations of sugary drink consumption and its substitution with alternative beverages with body weight gain among young children predisposed to future weight gain. Secondary analysis of the Healthy Start Study, a 1·5-year randomised controlled trial designed to prevent overweight among Danish children aged 2−6 years (n 366), was carried out. Multivariate linear regression models were used to investigate the associations of beverage consumption with change in body weight (Δweight) or BMI(ΔBMI) z-score. Substitution models were used to extrapolate the influence of replacing sugary drinks with alternative beverages (water, milk and diet drinks) on Δweight or ΔBMI z-score. Sugary drink intake at baseline and substitution of sugary drinks with milk were associated with both Δweight and ΔBMI z-score. Every 100 g/d increase in sugary drink intake was associated with 0·10 kg and 0·06 unit increases in body weight (P=0·048) and BMI z-score (P=0·04), respectively. Substitution of 100 g/d sugary drinks with 100 g/d milk was inversely associated with Δweight (β=−0·16 kg; P=0·045) and ΔBMI z-score (β=−0·07 units; P=0·04). The results of this study suggest that sugary drink consumption was associated with body weight gain among young children with high predisposition for future overweight. In line with the current recommendations, sugary drinks, whether high in added or natural sugar, should be discouraged to help prevent childhood obesity. Milk may be a good alternative to sugary drinks with regard to weight management among young obesity-predisposed children.

Results from previous studies on maternal folic acid intake and infant oral clefts are inconclusive. The aim of the present study was to investigate the association between women’s use of folic acid and/or multivitamin supplements and the risk for oral cleft in the newborn. We used data from the Medical Birth Registry of Norway based on all births in Norway from 1999 to 2013. A total of 528 220 women had 880 568 pregnancies, resulting in 896 674 live births and stillbirths, of which 1623 had oral clefts (isolated oral clefts, n 1311; non-isolated oral clefts, n 312). Altogether, 21·5 % of women were vitamin supplement users before pregnancy. The birth prevalence of oral clefts was 1·81/1000 live births and stillbirths. Relative risks (RR) were estimated with log-binomial regression. For pregnancies with maternal use of vitamins, the adjusted RR for clefts overall was 0·90 (95 % CI 0·79, 1·04). The adjusted RR for cleft palate only (n 586) was 0·84 (95 % CI 0·66, 1·06) and that for cleft lip with or without cleft palate (n 1037) was 0·94 (95 % CI 0·79, 1·13). Associations were stronger for cleft cases that occurred in combination with other malformations (adjusted RR 0·63; 95 % CI 0·45, 0·88), although vitamin supplements provided no protection against isolated clefts (adjusted RR 0·98; 95 % CI 0·84, 1·15). In conclusion, our study demonstrates no statistically significant association between vitamin use and isolated oral clefts. However, we found lower risk for oral clefts that occurred in combination with other malformations.

Evidence suggests that diets meeting recommendations for fruit and vegetable (F&V) intake are more costly. Dietary costs may be a greater constraint on the diet quality of people of lower socioeconomic position (SEP). The aim of this study was to examine whether dietary costs are more strongly associated with F&V intake in lower-SEP groups than in higher-SEP groups. Data on individual participants’ education and income were available from a population-based, cross-sectional study of 10 020 British adults. F&V intake and dietary costs (GBP/d) were derived from a semi-quantitative FFQ. Dietary cost estimates were based on UK food prices. General linear models were used to assess associations between SEP, quartiles of dietary costs and F&V intake. Effect modification of SEP gradients by dietary costs was examined with interaction terms. Analysis demonstrated that individuals with lowest quartile dietary costs, low income and low education consumed less F&V than individuals with higher dietary costs, high income and high education. Significant interaction between SEP and dietary costs indicated that the association between dietary costs and F&V intake was stronger for less-educated and lower-income groups. That is, socioeconomic differences in F&V intake were magnified among individuals who consumed lowest-cost diets. Such amplification of socioeconomic inequalities in diet among those consuming low-cost diets indicates the need to address food costs in strategies to promote healthy diets. In addition, the absence of socioeconomic inequalities for individuals with high dietary costs suggests that high dietary costs can compensate for lack of other material, or psychosocial resources.

Only one prospective study has analysed the relationship between the inflammatory properties of diet and risk of depression thus far. The aim of this study was to assess the association between the dietary inflammatory index (DII) and the incidence of depression. In a cohort study of 15 093 university graduates, participants completed a validated FFQ at baseline and after 10 years of follow-up. The DII was calculated based on the FFQ. Each of the twenty-eight nutrients or foods received a score based on findings from the peer-reviewed literature reporting on the relationships between diet and inflammatory biomarkers (IL-1β, IL-4, IL-6, IL-10, TNF-α and C-reactive protein). Participants were classified as having depression if they reported a new clinical diagnosis of depression by a physician, antidepressant drugs, or both. Multivariable Cox regression models were used to estimate hazard ratios (HR) of depression according to quintiles of the DII. After a median 8·5 years of follow-up, we observed 1051 incident cases of depression. The HR for participants in the highest quintile of DII (strongly pro-inflammatory) was 1·47 (95 % CI 1·17, 1·85) compared with those in the bottom quintile, with a significant dose–response relationship (Ptrend=0·01). In the subgroup analyses, the association between DII and depression was stronger among participants >55 years and among those with cardiometabolic comorbidities (HR 2·70; 95 % CI 1·22, 5·97 and HR 1·80; 95 % CI 1·27, 2·57, respectively). A pro-inflammatory diet was associated with a significantly higher risk of depression in a Mediterranean population. This association was stronger among older subjects and subjects with cardiometabolic diseases.

Prospective cohort studies have shown inverse associations between fibre intake and CVD, possibly mediated by blood pressure (BP). However, little is known about the impact of types of fibre on BP. We examined cross-sectional associations with BP of total, insoluble and soluble fibre intakes. Data were used from the INTERnational study on MAcro/micronutrients and blood Pressure (INTERMAP) study, including 2195 men and women aged between 40 and 59 years from the USA. During four visits, eight BP, four 24 h dietary recalls and two 24 h urine samples were collected. Linear regression models adjusted for lifestyle and dietary confounders to estimate BP differences per 2 sd higher intakes of total and individual types of fibre were calculated. After multivariable adjustment, total fibre intake higher by 6·8 g/4184 kJ (6·8 g/1000 kcal) was associated with a 1·69 mmHg lower systolic blood pressure (SBP; 95 % CI −2·97, −0·41) and attenuated to −1·01 mmHg (95 % CI −2·35, 0·34) after adjustment for urinary K. Insoluble fibre intake higher by 4·6 g/4184 kJ (4·6 g/1000 kcal) was associated with a 1·81 mmHg lower SBP (95 % CI −3·65, 0·04), additionally adjusted for soluble fibre and urinary K excretion, whereas soluble fibre was not associated with BP. Raw fruit was the main source of total and insoluble fibre, followed by whole grains and vegetables. In conclusion, higher intakes of fibre, especially insoluble, may contribute to lower BP, independent of nutrients associated with higher intakes of fibre-rich foods.

Areas with low, adequate and excessive I content in water co-exist in China. Limited data are currently available on I nutrition and thyroid disease in lactating women and their breast-fed infants with different I intakes. This study aimed to evaluate I nutrition in both lactating women and their infants and the prevalence of thyroid disease in areas with different levels of I in water. From January to June 2014, a total of 343 healthy lactating women (excluding those taking anti-thyroid drugs or I supplements within a year of the study, consuming seafood at the time of the study or those diagnosed with congenital thyroid disease) from Beihai in Guangxi province and Jiajiazhuang, Yangcheng, Jicun and Pingyao townships in Shanxi province were selected. Compared with the I-sufficient group, median urinary I concentrations in both lactating women and infants as well as breast milk I levels were significantly lower in the I-deficient group (P<0·001). The prevalence of thyroid disease in lactating women, particularly subclinical hypothyroidism, was higher in the I-excess group than in the I-sufficient group (P<0·05). In areas with excessive water I content, high thyroid peroxidase antibody and high thyroglobulin levels were risk factors for abnormal thyroid-stimulating hormone levels. Our data collectively suggest that excessive I intake potentially causes subclinical hypothyroidism in lactating women. Moreover, enhanced monitoring of I status is important to avoid adverse effects of I deficiency or excess, particularly in susceptible populations such as pregnant or lactating women and infants.

This study examines the relationship between long-term intake of six flavonoid classes and incidence of CVD and CHD, using a comprehensive flavonoid database and repeated measures of intake, while accounting for possible confounding by components of a healthy dietary pattern. Flavonoid intakes were assessed using a FFQ among the Framingham Offspring Cohort at baseline and three times during follow-up. Cox proportional hazards regression was used to characterise prospective associations between the natural logarithms of flavonoid intakes and CVD incidence using a time-dependent approach, in which intake data were updated at each examination to represent average intakes from previous examinations. Mean baseline age was 54 years, and 45 % of the population was male. Over an average 14·9 years of follow-up among 2880 participants, there were 518 CVD events and 261 CHD events. After multivariable adjustment, only flavonol intake was significantly associated with lower risk of CVD incidence (hazard ratios (HR) per 2·5-fold flavonol increase=0·86, Ptrend=0·05). Additional adjustment for total fruit and vegetable intake and overall diet quality attenuated this observation (HR=0·89, Ptrend=0·20 and HR=0·92, Ptrend=0·33, respectively). There were no significant associations between flavonoids and CHD incidence after multivariable adjustment. Our findings suggest that the observed association between flavonol intake and CVD risk may be a consequence of better overall diet. However, the strength of this non-significant association was also consistent with relative risks observed in previous meta-analyses, and therefore a modest benefit of flavonol intake on CVD risk cannot be ruled out.

Despite recent attempts to improve the quality of school meals in England through the introduction of school meal standards, uptake remains low. Since the introduction of the universal infant free school meal (UIFSM) scheme in September 2014 all pupils in Reception, Year 1 and Year 2 in English state-funded primary schools are eligible to receive a free lunch. This study aimed to explore the perceptions of pupils, catering managers and head teachers concerning school meal provision in eight primary schools in North England and provides a unique insight into each school’s preparation for implementation of UIFSM. A total of thirty-two focus groups were conducted with sixty-four pupils aged 7–8 years (Year 3) and sixty-four pupils aged 9–10 years (Year 5) in June–July 2014, to explore perceptions of school meals. Interviews were carried out with six catering managers and five head teachers concerning catering and the impending implementation of UIFSM. Increasing acceptance of school meals could lead to improved uptake. Pupils desired increased choice and menu variety, including greater variety of vegetables and fruit. Caterers can influence the quantity and types of foods offered to pupils, and there are opportunities for them to promote healthy eating behaviours in the dining room. The important roles of school meal providers, caterers, pupils and parents need to be recognised to improve delivery and acceptability of school meals and ultimately school meal uptake. There were practical challenges to implementation of UIFSM, with some concerns expressed over its feasibility. Head teachers were mainly positive about the potential beneficial impacts of the scheme.