Diets supplemented with fish oil (FO), which is rich in n-3 PUFA, have been shown to modify several key risk factors for CVD. The purpose of the present study was to determine the effect of FO supplementation on mitochondrial dynamic protein expression in the endothelium and on endothelial cell function. Male apoE-deficient (apoE− / −) mice (8 weeks old, n 12 per group) were fed a high-fat diet containing 45 % fat (HFD group) or a HFD with partial replacement of lard with 10 % (w/w) FO (FO group) (total EPA and DHA content 64·1 g/kg) for 8 weeks. ApoE− / − mice in the FO group had a greater endothelium-dependent vasorelaxation response to acetylcholine (Ach) than those in the HFD group. The atherosclerotic lesion volume in the aortic sinus of mice in the FO group was 54 % lower than that in the HFD group (P< 0·01). In addition, the aortas isolated from mice in the FO group had higher expression levels of Mfn2 and Opa1 but lower expression levels of Fis1 than those from the HFD group. Compared with mice fed the HFD, those fed the FO diet showed significantly lower levels of mitochondrial oxidative stress, cytochrome c release and caspase-3 activity (each P< 0·05). Furthermore, FO-fed mice displayed increased NO release and availability and enhanced endothelial NO synthase activity compared with HFD-fed mice. Taken together, these results reveal a novel mechanism by which FO protects against endothelial cell dysfunction, which may result in improved mitochondrial dynamics.

Exocrine pancreatic digestive enzymes are essential for the digestion of dietary components and are regulated by them. Chronic excess dietary high fat (HF) consumption is a contributing factor of diet-induced obesity (DIO) and associated chronic diseases and requires adaptation by the pancreas. The aim of the present study was to investigate the effects of chronic HF diet feeding on exocrine pancreatic digestive enzyme transcript levels in DIO C57BL/6J mice. C57BL/6J mice were fed diets containing either 10 or 45 % energy (E%) derived from fat for 12 weeks (n 10 mice per diet group). Pancreatic tissue and blood samples were collected at 0, 4 and 12 weeks. The expression of a panel of exocrine pancreatic digestive enzymes was analysed using quantitative RT-PCR and Western blot analysis. The HF (45 E%) diet-fed C57BL/6J mice developed obesity, hyperleptinaemia, hyperglycaemia and hyperinsulinaemia. The transcript levels of pancreatic lipase (PL), pancreatic lipase-related protein 2 (PLRP2) and pancreatic phospholipase A2 (PLA2) were initially elevated; however, they were down-regulated to basal control levels at week 12. The transcript levels of colipase were significantly affected by diet and time. The protein levels of PL and PLRP2 responded to HF diet feeding. The transcript levels of amylase and proteases were not significantly affected by diet and time. The transcript levels of specific lipases in hyperinsulinaemic, hyperleptinaemic and hyperglycaemic DIO C57BL/6J mice are down-regulated. However, these mice compensate for this by the post-transcriptional regulation of the levels of proteins that respond to dietary fat. This suggests a complex regulatory mechanism involved in the modulation of fat digestion.

Provitamin A biofortification of staple crops may decrease the prevalence of vitamin A (VA) deficiency if widely adopted in target countries. To assess the impact of processing methods on the VA value of plant foods, the unique bioefficacies of cis-βC isomers (formed during cooking) compared with all-trans (at) β-carotene (βC) must be determined. The bioefficacies of 9-cis (9c)- and 13-cis (13c)-βC isomers were compared with those of the at-βC isomer and VA positive (VA+) and negative (VA − ) controls in VA-depleted Mongolian gerbils (Meriones unguiculatus) in two experimental studies (study 1, n 56; study 2, n 57). A 3- or 4-week depletion period was followed by a 3- or 4-week treatment period in which the groups received oral doses of the 9c-, 13c- or at-βC isomers in cottonseed oil (study 1, 15 nmol/d; study 2, 30 nmol/d). In study 1, the βC isomers did not maintain baseline liver VA stores in all groups (0·69 (sd 0·20) μmol/liver) except in the VA+group (0·56 (sd 0·10) μmol/liver) (P= 0·0026). The βC groups were similar to the VA+group, but the 9c- and 13c-βC groups did not differ from the VA − group (0·39 (sd 0·09) μmol/liver). In study 2, the βC isomers maintained baseline liver VA stores in all the βC groups (0·35 (sd 0·13) μmol/liver), and in the VA+group, the VA supplement (0·54 (sd 0·19) μmol/liver) exceeded the baseline VA status (0·38 (sd 0·15) μmol/liver) (P< 0·0001); however, the 9c-βC group did not differ from the VA − group (0·20 (sd 0·07) μmol/liver). In vivo isomerisation of βC was confirmed in both experimental studies. Lower VA bioconversion factor values were obtained for the cis-βC isomers in study 2 when compared with study 1, but higher values were obtained for the at-βC isomer. Dose and VA status clearly affect bioconversion factors. In conclusion, the cis-βC isomers yielded similar liver VA stores to the at-βC isomer in Mongolian gerbils, and liver VA stores of the 9c- and 13c-βC groups did not differ when the doses were provided at physiological levels over time in two studies.

In the present study, three primiparous lactating Holstein cows (260–285 d in lactation) were used in a 3 × 3 Latin square design to assess the effects of three doses (0·0, 0·4 and 0·8 μg/kg body weight) of lipopolysaccharide (LPS, Escherichia coli 0111:B4) on changes in ruminal microbiota and ruminal fermentation. Ruminal pH was linearly decreased (P< 0·001) by LPS challenge, and the concentrations of acetate, propionate, butyrate, total volatile fatty acids and amino N increased linearly (P< 0·001) according to the LPS dose. LPS infusion linearly decreased (P< 0·001) the organic matter degradability of alfalfa hay and soyabean meal in the rumen, but did not affect (P>0·10) the gene expression of Na+/K+-ATPase and monocarboxylic acid transporter-1, -2 and -4. A plot of principal coordinate analysis based on unweighted UniFrac values and analysis of molecular variance revealed that the structure of ruminal bacterial communities in the control was distinct from that of the ruminal microbiota in the cattle exposed to LPS. At the phylum level, when compared with the control group, LPS infusion in the tested cows linearly increased (P< 0·05) the abundance of Firmicutes, and linearly decreased (P< 0·05) the percentage of Bacteroidetes, Tenericutes, Spirochaetes, Chlorobi and Lentisphaerae. To our knowledge, this is the first study to report that intravenously LPS challenge altered the ruminal bacterial microbiota and fermentation profiles. The present data suggest that systemic LPS could alter ruminal environment and ruminal microbiota composition, leading to a general decrease in fermentative activity.

Overconsumption of sugar-sweetened beverages has been implicated in the pathogenesis of CVD. The objective of the present study was to elucidate acute haemodynamic and microcirculatory responses to the ingestion of sugary drinks made from sucrose, glucose or fructose at concentrations similar to those often found in commercial soft drinks. In a randomised cross-over study design, twelve young healthy human subjects (seven men) ingested 500 ml tap water in which was dissolved 60 g of either sucrose, glucose or fructose, or an amount of fructose equivalent to that present in sucrose (i.e. 30 g fructose). Continuous cardiovascular monitoring was performed for 30 min before and at 60 min after ingestion of sugary drinks, and measurements included beat-to-beat blood pressure (BP) and impedance cardiography. Additionally, microvascular endothelial function testing was performed after iontophoresis of acetylcholine and sodium nitroprusside using laser Doppler flowmetry. Ingestion of fructose (60 or 30 g) increased diastolic and mean BP to a greater extent than the ingestion of 60 g of either glucose or sucrose (P< 0·05). Ingestion of sucrose and glucose increased cardiac output (CO; P< 0·05), index of contractility (P< 0·05) and stroke volume (P< 0·05), but reduced total peripheral resistance (TPR; P< 0·05), which contrasts with the tendency of fructose (60 and 30 g) to increase resistance. Microvascular endothelial function did not differ in response to the ingestion of various sugary drinks. In conclusion, ingestion of fructose, but not sucrose, increases BP in healthy human subjects. Although sucrose comprises glucose and fructose, its changes in TPR and CO are more related to glucose than to fructose.

It has been suggested that vitamin D2 is not very prevalent in the human food chain. However, data from a number of recent intervention studies suggest that the majority of subjects had measurable serum 25-hydroxyvitamin D2 (25(OH)D2) concentrations. Serum 25(OH)D2, unlike 25(OH)D3, is not directly influenced by exposure of skin to sun and thus has dietary origins; however, quantifying dietary vitamin D2 is difficult due to the limitations of food composition data. Therefore, the present study aimed to characterise serum 25(OH)D2 concentrations in the participants of the National Adult Nutrition Survey (NANS) in Ireland, and to use these serum concentrations to estimate the intake of vitamin D2 using a mathematical modelling approach. Serum 25(OH)D2 concentration was measured by a liquid chromatography–tandem MS method, and information on diet as well as subject characteristics was obtained from the NANS. Of these participants, 78·7 % (n 884) had serum 25(OH)D2 concentrations above the limit of quantification, and the mean, maximum, 10th, 50th (median) and 90th percentile values of serum 25(OH)D2 concentrations were 3·69, 27·6, 1·71, 2·96 and 6·36 nmol/l, respectively. To approximate the intake of vitamin D2 from these serum 25(OH)D2 concentrations, we used recently published data on the relationship between vitamin D intake and the responses of serum 25(OH)D concentrations. The projected 5th to 95th percentile intakes of vitamin D2 for adults were in the range of 0·9–1·2 and 5–6 μg/d, respectively, and the median intake ranged from 1·7 to 2·3 μg/d. In conclusion, the present data demonstrate that 25(OH)D2 concentrations are present in the sera of adults from this nationally representative sample. Vitamin D2 may have an impact on nutritional adequacy at a population level and thus warrants further investigation.

Previous research has shown that resveratrol can increase cerebral blood flow (CBF) in the absence of improved cognitive performance in healthy, young human subjects during the performance of cognitively demanding tasks. This lack of cognitive effects may be due to low bioavailability and, in turn, reduced bioefficacy of resveratrol in vivo. Piperine can alter polyphenol pharmacokinetics, but previous studies have not investigated whether this affects the efficacy of the target compound. Therefore, the objective of the present study was to ascertain whether co-supplementation of piperine with resveratrol affects the bioavailability and efficacy of resveratrol with regard to cognition and CBF. The present study utilised a randomised, double-blind, placebo-controlled, within-subjects design, where twenty-three adults were given placebo, trans-resveratrol (250 mg) and trans-resveratrol with 20 mg piperine on separate days at least a week apart. After a 40 min rest/absorption period, the participants performed a selection of cognitive tasks and CBF was assessed throughout the period, in the frontal cortex, using near-IR spectroscopy. The presence of resveratrol and its conjugates in the plasma was confirmed by liquid chromatography–MS analysis carried out following the administration of the same doses in a separate cohort (n 6). The results indicated that when co-supplemented, piperine and resveratrol significantly augmented CBF during task performance in comparison with placebo and resveratrol alone. Cognitive function, mood and blood pressure were not affected. The plasma concentrations of resveratrol and its metabolites were not significantly different between the treatments, which indicates that co-supplementation of piperine with resveratrol enhances the bioefficacy of resveratrol with regard to CBF effects, but not cognitive performance, and does this without altering bioavailability.

Phytosterols (PS, comprising plant sterols and plant stanols) have been proven to lower LDL-cholesterol concentrations. The dose–response relationship for this effect has been evaluated in several meta-analyses by calculating averages for different dose ranges or by applying continuous dose–response functions. Both approaches have advantages and disadvantages. So far, the calculation of averages for different dose ranges has not been done for plant sterols and stanols separately. The objective of the present meta-analysis was to investigate the combined and separate effects of plant sterols and stanols when classified into different dose ranges. Studies were searched and selected based on predefined criteria. Relevant data were extracted. Average LDL-cholesterol effects were calculated when studies were categorised by dose, according to random-effects models while using the variance as weighing factor. This was done for plant sterols and stanols combined and separately. In total, 124 studies (201 strata) were included. Plant sterols and stanols were administered in 129 and fifty-nine strata, respectively; the remaining used a mix of both. The average PS dose was 2·1 (range 0·2–9·0) g/d. PS intakes of 0·6–3·3 g/d were found to gradually reduce LDL-cholesterol concentrations by, on average, 6–12 %. When plant sterols and stanols were analysed separately, clear and comparable dose–response relationships were observed. Studies carried out with PS doses exceeding 4 g/d were not pooled, as these were scarce and scattered across a wide range of doses. In conclusion, the LDL-cholesterol-lowering effect of both plant sterols and stanols continues to increase up to intakes of approximately 3 g/d to an average effect of 12 %.

Recent studies have implicated Ca supplements in vascular risk elevation, and therefore these supplements may also be associated with the occurrence of brain lesions (or hyperintensities) in older adults. These lesions represent damage to brain tissue that is caused by ischaemia. In the present cross-sectional clinical observational study, the association between Ca-containing dietary supplement use and lesion volumes was investigated in a sample of 227 older adults (60 years and above). Food and supplemental Ca intakes were assessed with the Block 1998 FFQ; participants with supplemental Ca intake above zero were categorised as supplement users. Lesion volumes were determined from cranial MRI (1·5 tesla) scans using a semi-automated technique; volumes were log-transformed because they were non-normal. ANCOVA models revealed that supplement users had greater lesion volumes than non-users, even after controlling for food Ca intake, age, sex, race, years of education, energy intake, depression and hypertension (Ca supplement use: β = 0·34, se 0·10, F1,217= 10·98, P= 0·0011). The influence of supplemental Ca use on lesion volume was of a magnitude similar to that of the influence of hypertension, a well-established risk factor for lesions. Among the supplement users, the amount of supplemental Ca was not associated with lesion volume (β = − 0·000035, se 0·00 015, F1,139= 0·06, P= 0·81). The present study demonstrates that the use of Ca-containing dietary supplements, even low-dose supplements, by older adults may be associated with greater lesion volumes. Evaluation of randomised controlled trials is warranted to determine whether this relationship is a causal one.

Dietary intake is a modifiable exposure that may have an impact on cognitive outcomes in older age. The long-term aetiology of cognitive decline and dementia, however, suggests that the relevance of dietary intake extends across the lifetime. In the present study, we tested whether retrospective dietary patterns from the life periods of childhood, early adulthood, adulthood and middle age predicted cognitive performance in a cognitively healthy sample of 352 older Australian adults >65 years. Participants completed the Lifetime Diet Questionnaire and a battery of cognitive tests designed to comprehensively assess multiple cognitive domains. In separate regression models, lifetime dietary patterns were the predictors of cognitive factor scores representing ten constructs derived by confirmatory factor analysis of the cognitive test battery. All regression models were progressively adjusted for the potential confounders of current diet, age, sex, years of education, English as native language, smoking history, income level, apoE ɛ4 status, physical activity, other past dietary patterns and health-related variables. In the adjusted models, lifetime dietary patterns predicted cognitive performance in this sample of older adults. In models additionally adjusted for intake from the other life periods and mechanistic health-related variables, dietary patterns from the childhood period alone reached significance. Higher consumption of the ‘coffee and high-sugar, high-fat extras’ pattern predicted poorer performance on simple/choice reaction time, working memory, retrieval fluency, short-term memory and reasoning. The ‘vegetable and non-processed’ pattern negatively predicted simple/choice reaction time, and the ‘traditional Australian’ pattern positively predicted perceptual speed and retrieval fluency. Identifying early-life dietary antecedents of older-age cognitive performance contributes to formulating strategies for delaying or preventing cognitive decline.

Cancer is a leading cause of death, and the dietary pattern in Korea is changing rapidly from a traditional Korean diet to a Westernised diet. In the present study, we investigated the effects of dietary factors on cancer risk with a prospective cohort study. Among 26 815 individuals who participated in cancer screening examinations from September 2004 to December 2008, 8024 subjects who completed a self-administered questionnaire concerning demographic and lifestyle factors, and a 3 d food record were selected. As of September 2013, 387 cancer cases were identified from the National Cancer Registry System, and the remaining individuals were included in the control group. The hazard ratio (HR) of cancer for the subjects older than or equal to 50 years of age was higher (HR 1·80, 95 % CI 1·41, 2·31; P< 0·0001) than that for the other subjects. Red meat consumption, Na intake and obesity (BMI ≥ 25 kg/m2) were positively associated with overall cancer incidence in men (HR 1·41, 95 % CI 1·02, 1·94; P= 0·0382), gastric cancer (HR 2·34, 95 % CI 1·06, 5·19; P= 0·0365) and thyroid cancer (HR 1·56, 95 % CI 1·05, 2·31; P= 0·0270), respectively. Participants who had at least three dietary risk factors among the high intakes of red meat and Na, low intakes of vegetables and fruits, and obesity suggested by the World Cancer Research Fund/American Institute for Cancer Research at baseline tended to have a higher risk of cancer than the others (HR 1·26, 95 % CI 0·99, 1·60; P= 0·0653). In summary, high intakes of red meat and Na were significant risk factors of cancer among Koreans.

Increasing evidence suggests that the Mediterranean diet can reduce the risk of CVD. Olive oil is the hallmark of this dietary pattern. We conducted a meta-analysis of case–control, prospective cohort studies and a randomised controlled trial investigating the specific association between olive oil consumption and the risk of CHD (101 460 participants) or stroke (38 673 participants). The results of all observational studies were adjusted for total energy intake. The random-effects model assessing CHD as an outcome showed a relative risk (RR) of 0·73 (95 % CI 0·44, 1·21) in case–control studies and 0·96 (95 % CI 0·78, 1·18) in cohort studies for a 25 g increase in olive oil consumption. In cohort studies, the random-effects model assessing stroke showed a RR of 0·74 (95 % CI 0·60, 0·92). The random-effects model combining all cardiovascular events (CHD and stroke) showed a RR of 0·82 (95 % CI 0·70, 0·96). Evidence of heterogeneity was apparent for CHD, but not for stroke. Both the Egger test (P= 0·06) and the funnel plot suggested small-study effects. Available studies support an inverse association of olive oil consumption with stroke (and with stroke and CHD combined), but no significant association with CHD. This finding is in agreement with the recent successful results of the PREDIMED randomised controlled trial.

Findings from research that has assessed the influence of dietary factors on child obesity have been equivocal. In the present study, we aimed to test the hypothesis that a positive change in diet quality is associated with favourable changes in BMI z-scores (zBMI) in schoolchildren from low socio-economic backgrounds and to examine whether this effect is modified by BMI category at baseline. The present study utilised data from a subsample (n 216) of the Resilience for Eating and Activity Despite Inequality study, a longitudinal cohort study with data collected in 2007–8 (T1) and 2010–11 (T2) in socio-economically disadvantaged women and children (5–12 years at T1). Dietary data were collected using a FFQ and diet quality index (DQI) scores derived at both time points. The objective measures of weight, height and physical activity (accelerometers) were included. The other variables were reported in the questionnaires. We examined the association between change in DQI and change in zBMI, using linear regression analyses adjusted for physical activity, screen sedentary behaviour and maternal education level both in the whole sample and in the sample stratified by overweight status at baseline. After accounting for potential covariates, change in diet quality was found to be inversely associated with change in zBMI only in children who were overweight at baseline (P= 0·035), thus supporting the hypothesis that improvement in diet quality is associated with a concurrent improvement in zBMI among already overweight children, but not among those with a normal BMI status. The identification of modifiable behaviours such as diet quality that affect zBMI longitudinally is valuable to inform future weight gain prevention interventions in vulnerable groups.

Few studies have investigated the relative validity of FFQ in young children and no study has investigated the relative validity of changes in children's food intake in a longitudinal context. The aim of the present study was to compare the FFQ of the longitudinal Family Influences on Food Intake study, assessing children's food intake in the previous 3 months, with a 3 d online food record when children were 3 and 7 years old, as well as to investigate the relative validity of changes in food group intake over a 4-year period. Parents (n 89) completed the FFQ and an online food record over three non-consecutive days on two separate occasions (January–April 2008 and 2012). Wilcoxon signed-rank tests and Spearman's correlations were used to compare food group intake and changes in intake assessed using both methods. In 2008, the intake of eleven of the twenty-two food groups was overestimated and that of four food groups underestimated in the FFQ in comparison with the online tool; in 2012, the intake of four food groups was overestimated and that of seven food groups underestimated. Nevertheless, changes in intake did not differ significantly between the two methods for eighteen food groups. Correlations in 2008 and 2012 were, on average, 0·47; correlations between the changes in dietary intake were, on average, 0·26. The results suggest that despite the significant differences between the two methods for a number of food groups at both baseline and/or follow-up, the FFQ can be used to monitor changes in dietary intake for groups of young children.

Food-based dietary recommendations (FBR) play an essential role in promoting a healthy diet. To support the process of formulating a set of population-specific FBR, a probabilistic model was developed specifically to predict the changes in the percentage of a population at risk of inadequate nutrient intakes after the adoption of alternative sets of FBR. The model simulates the distribution of the number of servings per week from food groups or food items at baseline and after the hypothetical successful adoption of alternative sets of FBR, while ensuring that the population's energy intake distribution remains similar. The simulated changes from baseline in median nutrient intakes and the percentage of the population at risk of inadequate nutrient intakes are calculated and compared across the alternative sets of FBR. The model was illustrated using a hypothetical population of 12- to 18-month-old breast-feeding children consuming a cereal-based diet low in animal source foods.