The importance of chronic low-grade inflammation in the pathology of numerous age-related chronic conditions is now clear. An unresolved inflammatory response is likely to be involved from the early stages of disease development. The present position paper is the most recent in a series produced by the International Life Sciences Institute's European Branch (ILSI Europe). It is co-authored by the speakers from a 2013 workshop led by the Obesity and Diabetes Task Force entitled ‘Low-grade inflammation, a high-grade challenge: biomarkers and modulation by dietary strategies’. The latest research in the areas of acute and chronic inflammation and cardiometabolic, gut and cognitive health is presented along with the cellular and molecular mechanisms underlying inflammation–health/disease associations. The evidence relating diet composition and early-life nutrition to inflammatory status is reviewed. Human epidemiological and intervention data are thus far heavily reliant on the measurement of inflammatory markers in the circulation, and in particular cytokines in the fasting state, which are recognised as an insensitive and highly variable index of tissue inflammation. Potential novel kinetic and integrated approaches to capture inflammatory status in humans are discussed. Such approaches are likely to provide a more discriminating means of quantifying inflammation–health/disease associations, and the ability of diet to positively modulate inflammation and provide the much needed evidence to develop research portfolios that will inform new product development and associated health claims.

The number of known glucose transporters has expanded considerably over the past 2 years. At least three, and up to six, Na+-dependent glucose transporters (SGLT1–SGLT6; gene name SLC5A) have been identified. Similarly, thirteen members of the family of facilitative sugar transporters (GLUT1–GLUT12 and HMIT; gene name SLC2A) are now recognised. These various transporters exhibit different substrate specificities, kinetic properties and tissue expression profiles. The number of distinct gene products, together with the presence of several different transporters in certain tissues and cells (for example, GLUT1, GLUT4, GLUT5, GLUT8, GLUT12 and HMIT in white adipose tissue), indicates that glucose delivery into cells is a process of considerable complexity.

Vitamin D is metabolised by a hepatic 25-hydroxylase into 25-hydroxyvitamin D (25(OH)D) and by a renal 1α-hydroxylase into the vitamin D hormone calcitriol. Calcitriol receptors are present in more than thirty different tissues. Apart from the kidney, several tissues also possess the enzyme 1α-hydroxylase, which is able to use circulating 25(OH)D as a substrate. Serum levels of 25(OH)D are the best indicator to assess vitamin D deficiency, insufficiency, hypovitaminosis, adequacy, and toxicity. European children and young adults often have circulating 25(OH)D levels in the insufficiency range during wintertime. Elderly subjects have mean 25(OH)D levels in the insufficiency range throughout the year. In institutionalized subjects 25(OH)D levels are often in the deficiency range. There is now general agreement that a low vitamin D status is involved in the pathogenesis of osteoporosis. Moreover, vitamin D insufficiency can lead to a disturbed muscle function. Epidemiological data also indicate a low vitamin D status in tuberculosis, rheumatoid arthritis, multiple sclerosis, inflammatory bowel diseases, hypertension, and specific types of cancer. Some intervention trials have demonstrated that supplementation with vitamin D or its metabolites is able: (i) to reduce blood pressure in hypertensive patients; (ii) to improve blood glucose levels in diabetics; (iii) to improve symptoms of rheumatoid arthritis and multiple sclerosis. The oral dose necessary to achieve adequate serum 25(OH)D levels is probably much higher than the current recommendations of 5–15 μg/d.

The extent to which women of reproductive age are able to convert the n−3 fatty acid α-linolenic acid (ALNA) to eicosapentaenoic acid (EPA), docosapentaenoic acid (DPA) and docosahexaenoic acid (DHA) was investigated in vivo by measuring the concentrations of labelled fatty acids in plasma for 21 d following the ingestion of [U−13C]ALNA (700 mg). [13C]ALNA excursion was greatest in cholesteryl ester (CE) (224 (SEM 70) μmol/l over 21 d) compared with triacylglycerol (9-fold), non-esterified fatty acids (37-fold) and phosphatidylcholine (PC, 7-fold). EPA excursion was similar in both PC (42 (SEM 8) μmol/l) and CE (42 (SEM 9) μmol/l) over 21 d. In contrast both [13C]DPA and [13C]DHA were detected predominately in PC (18 (SEM 4) and 27 (SEM 7) μmol/l over 21 d, respectively). Estimated net fractional ALNA inter-conversion was EPA 21 %, DPA 6 % and DHA 9 %. Approximately 22 % of administered [13C]ALNA was recovered as 13CO2 on breath over the first 24 h of the study. These results suggest differential partitioning of ALNA, EPA and DHA between plasma lipid classes, which may facilitate targeting of individual n−3 fatty acids to specific tissues. Comparison with previous studies suggests that women may possess a greater capacity for ALNA conversion than men. Such metabolic capacity may be important for meeting the demands of the fetus and neonate for DHA during pregnancy and lactation. Differences in DHA status between women both in the non-pregnant state and in pregnancy may reflect variations in metabolic capacity for DHA synthesis.

Vitamin D deficiency is associated with osteoporosis and is thought to increase the risk of cancer and CVD. Despite these numerous potential health effects, data on vitamin D status at the population level and within key subgroups are limited. The aims of the present study were to examine patterns of 25-hydroxyvitamin D (25(OH)D) levels worldwide and to assess differences by age, sex and region. In a systematic literature review using the Medline and EMBASE databases, we identified 195 studies conducted in forty-four countries involving more than 168 000 participants. Mean population-level 25(OH)D values varied considerably across the studies (range 4·9–136·2 nmol/l), with 37·3 % of the studies reporting mean values below 50 nmol/l. The highest 25(OH)D values were observed in North America. Although age-related differences were observed in the Asia/Pacific and Middle East/Africa regions, they were not observed elsewhere and sex-related differences were not observed in any region. Substantial heterogeneity between the studies precluded drawing conclusions on overall vitamin D status at the population level. Exploratory analyses, however, suggested that newborns and institutionalised elderly from several regions worldwide appeared to be at a generally higher risk of exhibiting lower 25(OH)D values. Substantial details on worldwide patterns of vitamin D status at the population level and within key subgroups are needed to inform public health policy development to reduce risk for potential health consequences of an inadequate vitamin D status.

Following the publication of the landmark trial of Clark et al. in 1996 that appeared to show that Se could reduce the risk of cancer, awareness of the importance of Se to human health has markedly increased. As a result, there is now much more aggressive marketing of Se supplements and functional foods, even in situations where additional consumption of Se is inappropriate. The present review addresses how Se gets into the food chain, the wide variability in Se content of foods and the very different levels of intake between countries and regions. Though it is clear that there are adverse consequences for health of both deficient and excessive intake, health effects at intermediate levels of intake are less certain. Thus it is difficult to define optimal intake which depends on a large number of factors, such as which functions of Se are most relevant to a particular disease state, which species of Se is most prominent in the Se source, which health condition is being considered, the adequacy or otherwise of intake of other nutrients, the presence of additional stressors, and lastly whether the ability to make selenoproteins may be compromised. These complexities need to be understood, particularly by policy makers, in order to make informed judgments. Potential solutions for increasing Se intake, where required, include agronomic biofortification and genetic biofortification or, for individuals, increased intake of naturally Se-rich foods, functional foods or supplements. The difficulties of balancing the risks and benefits in relation to Se intake are highlighted.

Prebiotics are food ingredients that improve health by modulating the colonic microbiota. The bifidogenic effect of the prebiotic inulin is well established; however, it remains unclear which species of Bifidobacterium are stimulated in vivo and whether bacterial groups other than lactic acid bacteria are affected by inulin consumption. Changes in the faecal microbiota composition were examined by real-time PCR in twelve human volunteers after ingestion of inulin (10 g/d) for a 16-d period in comparison with a control period without any supplement intake. The prevalence of most bacterial groups examined did not change after inulin intake, although the low G+C % Gram-positive species Faecalibacterium prausnitzii exhibited a significant increase (10·3 % for control period v. 14·5 % during inulin intake, P = 0·019). The composition of the genus Bifidobacterium was studied in four of the volunteers by clone library analysis. Between three and five Bifidobacterium spp. were found in each volunteer. Bifidobacterium adolescentis and Bifidobacterium longum were present in all volunteers, and Bifidobacterium pseudocatenulatum, Bifidobacterium animalis, Bifidobacterium bifidum and Bifidobacterium dentium were also detected. Real-time PCR was employed to quantify the four most prevalent Bifidobacterium spp., B. adolescentis, B. longum, B. pseudocatenulatum and B. bifidum, in ten volunteers carrying detectable levels of bifidobacteria. B. adolescentis showed the strongest response to inulin consumption, increasing from 0·89 to 3·9 % of the total microbiota (P = 0·001). B. bifidum was increased from 0·22 to 0·63 % (P < 0·001) for the five volunteers for whom this species was present.

Women (n 160) aged 50 to 65 years were asked to weigh their food for 4 d on four occasions over the period of 1 year, using the PETRA (Portable Electronic Tape Recorded Automatic) scales. Throughout the year, they were asked to complete seven other dietary assessment methods: a simple 24 h recall, a structured 24 h recall with portion size assessments using photographs, two food-frequency questionnaires, a 7 d estimated record or open-ended food diary, a structured food-frequency (menu) record, and a structured food-frequency (menu) record with portion sizes assessed using photographs. Comparisons between the average of the 16 d weighed records and the first presentation of each method indicated that food-frequency questionnaires were not appreciably better at placing individuals in the distribution of habitual diet than 24 h recalls, due partly to inaccuracies in the estimation of frequency of food consumption. With a 7 d estimated record or open-ended food diary, however, individual values of nutrients were most closely associated with those obtained from 16 d weighed records, and there were no significant differences in average food or nutrient intakes.

Protein, generally agreed to be the most satiating macronutrient, may differ in its effects on appetite depending on the protein source and variation in digestion and absorption. We investigated the effects of two milk protein types, casein and whey, on food intake and subjective ratings of hunger and fullness, and on postprandial metabolite and gastrointestinal hormone responses. Two studies were undertaken. The first study showed that energy intake from a buffet meal ad libitum was significantly less 90 min after a 1700 kJ liquid preload containing 48 g whey, compared with an equivalent casein preload (P<0·05). In the second study, the same whey preload led to a 28 % increase in postprandial plasma amino acid concentrations over 3 h compared with casein (incremental area under the curve (iAUC), P<0·05). Plasma cholecystokinin (CCK) was increased by 60 % (iAUC, P<0·005), glucagon-like peptide (GLP)-1 by 65 % (iAUC, P<0·05) and glucose-dependent insulinotropic polypeptide by 36 % (iAUC, P<0·01) following the whey preload compared with the casein. Gastric emptying was influenced by protein type as evidenced by differing plasma paracetamol profiles with the two preloads. Greater subjective satiety followed the whey test meal (P<0·05). These results implicate post-absorptive increases in plasma amino acids together with both CCK and GLP-1 as potential mediators of the increased satiety response to whey and emphasise the importance of considering the impact of protein type on the appetite response to a mixed meal.

The role of very-low-carbohydrate ketogenic diets (VLCKD) in the long-term management of obesity is not well established. The present meta-analysis aimed to investigate whether individuals assigned to a VLCKD (i.e. a diet with no more than 50 g carbohydrates/d) achieve better long-term body weight and cardiovascular risk factor management when compared with individuals assigned to a conventional low-fat diet (LFD; i.e. a restricted-energy diet with less than 30 % of energy from fat). Through August 2012, MEDLINE, CENTRAL, ScienceDirect, Scopus, LILACS, SciELO, ClinicalTrials.gov and grey literature databases were searched, using no date or language restrictions, for randomised controlled trials that assigned adults to a VLCKD or a LFD, with 12 months or more of follow-up. The primary outcome was body weight. The secondary outcomes were TAG, HDL-cholesterol (HDL-C), LDL-cholesterol (LDL-C), systolic and diastolic blood pressure, glucose, insulin, HbA1c and C-reactive protein levels. A total of thirteen studies met the inclusion/exclusion criteria. In the overall analysis, five outcomes revealed significant results. Individuals assigned to a VLCKD showed decreased body weight (weighted mean difference − 0·91 (95 % CI − 1·65, − 0·17) kg, 1415 patients), TAG (weighted mean difference − 0·18 (95 % CI − 0·27, − 0·08) mmol/l, 1258 patients) and diastolic blood pressure (weighted mean difference − 1·43 (95 % CI − 2·49, − 0·37) mmHg, 1298 patients) while increased HDL-C (weighted mean difference 0·09 (95 % CI 0·06, 0·12) mmol/l, 1257 patients) and LDL-C (weighted mean difference 0·12 (95 % CI 0·04, 0·2) mmol/l, 1255 patients). Individuals assigned to a VLCKD achieve a greater weight loss than those assigned to a LFD in the long term; hence, a VLCKD may be an alternative tool against obesity.

Increasing evidence suggests that high consumption of ultra-processed foods (UPF) is associated with an increase in non-communicable diseases, overweight and obesity. The present study systematically reviewed all observational studies that investigated the association between UPF consumption and health status. A comprehensive search of MEDLINE, Embase, Scopus, Web of Science and Google Scholar was conducted, and reference lists of included articles were checked. Only cross-sectional and prospective cohort studies were included. At the end of the selection process, twenty-three studies (ten cross-sectional and thirteen prospective cohort studies) were included in the systematic review. As regards the cross-sectional studies, the highest UPF consumption was associated with a significant increase in the risk of overweight/obesity (+39 %), high waist circumference (+39 %), low HDL-cholesterol levels (+102 %) and the metabolic syndrome (+79 %), while no significant associations with hypertension, hyperglycaemia or hypertriacylglycerolaemia were observed. For prospective cohort studies evaluating a total population of 183 491 participants followed for a period ranging from 3·5 to 19 years, highest UPF consumption was found to be associated with increased risk of all-cause mortality in five studies (risk ratio (RR) 1·25, 95 % CI 1·14, 1·37; P < 0·00001), increased risk of CVD in three studies (RR 1·29, 95 % CI 1·12, 1·48; P = 0·0003), cerebrovascular disease in two studies (RR 1·34, 95 % CI 1·07, 1·68; P = 0·01) and depression in two studies (RR 1·20, 95 % CI 1·03, 1·40; P = 0·02). In conclusion, increased UPF consumption was associated, although in a limited number of studies, with a worse cardiometabolic risk profile and a higher risk of CVD, cerebrovascular disease, depression and all-cause mortality.

Inulin is a generic term to cover all β(2 → 1) linear fructans. Chicory inulin is a linear β(2 → 1) fructan (degree of polymerisation (DP) 2 to 60; DPav = 12), its partial enzymatic hydrolysis product is oligofructose (DP 2 to 8; DPav = 4), and by applying specific separation technologies a long-chain inulin knownas inulin HP (DP 10 to 60; DPav = 25) can be produced. Finally, a specific product known as oligofructose-enriched inulin is obtained by combining chicorylong-chain inulin and oligofructose. Because of the b-configuration of the anomeric C2 in their fructose monomers, inulin-type fructans resist hydrolysis byintestinal digestive enzymes, they classify as ‘non-digestible’ carbohydrates, and they are dietary fibres. By increasing faecal biomass and water content ofthe stools, they improve bowel habits, but they have characteristic features different from other fibres. They affect gastrointestinal functions not because oftheir physico-chemical properties but rather because of their biochemical and physiological attributes. In the colon, they are rapidly fermented to produceSCFA that are good candidates to explain some of the systemic effects of inulin-type fructans. Fermentation of inulin-type fructans in the large bowel is aselective process; bifidobacteria (and possibly a few other genera) are preferentially stimulated to grow, thus causing significant changes in the compositionof the gut microflora by increasing the number of potentially health-promoting bacteria and reducing the number of potentially harmful species. Both oligofructosead inulin are prebiotic. They also induce changes in colonic epithelium stimulating proliferation in the crypts, increasing the concentration ofpolyamines, changing the profile of mucins, and modulating endocrine as well as immune functions. From a nutrition labelling perspective, inulin-typefructans are not only prebiotic dietary fibres; they are also low-calorie carbohydrates [6·3 kJ/g (1·5 kcal/g)]. Supported by the results of a large numberof animal studies and human nutrition intervention trials, the claim ‘inulin-type fructans enhance calcium and magnesium absorption‘ is scientifically substantiated, but different inulin-type fructans have probably a different efficacy (in terms of effective daily dose), the most active product being the oligofructose-enriched inulin. A series of animal studies demonstrate that inulin-type fructans affect the metabolism of lipids primarily by decreasingtriglyceridaemia because of a reduction in the number of plasma VLDL particles. The human data largely confirm the animal experiments. They demonstratemainly a reduction in triglyceridaemia and only a relatively slight decrease in cholesterolaemia mostly in (slightly) hypertriglyceridaemic conditions. Inulinappears thus eligible for an enhanced function claim related to normalization of blood triacylglycerols. A large number of animal data convincingly showthat inulin-type fructans reduce the risk of colon carcinogenesis and nutrition intervention trials are now performed to test that hypothesis in human subjectsknown to be at risk for polyps and cancer development in the large bowel.

This paper assesses critically the science base that underpins the argument that oxidative damage is a significant causative factor in the development of human diseases and that antioxidants are capable of preventing or ameliorating these disease processes. The assessment has been carried out under a number of headings, and some recommendations for future research are made based on the present day knowledge base.

Techniques have been developed to produce microbial phytase for addition to diets for simple-stomached animals, with the aim to improve phosphorus availability from phytate-P in plant sources. The activity of the crude microbial phytase showed pH optima at pH 5.5 and 2.5. The enzyme was able to degrade phytate in vitro in soya-bean meal, maize and a liquid compound feed for pigs. When microbial phytase was added to low-P diets for broilers the availability of P increased to over 60% and the amount of P in the droppings decreased by 50%. The growth rate and feed conversion ratio on the low-P diets containing microbial phytase were comparable to or even better than those obtained on control diets. Addition of microbial phytase to diets for growing pigs increased the apparent absorbability of P by 24%. The amount of P in the faeces was 35% lower.

The literature on predefined indexes of overall diet quality is reviewed. Their association with nutrient adequacy and health outcome is considered, but our primary interest is in the make-up of the scores. In total, twenty different indexes have been reviewed, four of which have gained most attention, and many others were based on those four. The various scores differ in many respects, such as the items included, the cut-off values used, and the exact method of scoring, indicating that many arbitrary choices have been made. Correlations in intake between dietary components may not be adequately addressed. In general, diet quality scores show an association with mortality or disease risk, but these relations are generally modest. Existing indexes do not predict morbidity or mortality significantly better than individual dietary factors. Although conclusions from the review may provide guidance in the construction of a diet quality score, it is questionable whether a dietary score can be obtained that is a much better predictor of health outcome.

Although resveratrol has widely been studied for its potential health benefits, little is known about its metabolic effects in humans. Our aims were to determine whether the polyphenol resveratrol improves insulin sensitivity in type 2 diabetic patients and to gain some insight into the mechanism of its action. After an initial general examination (including blood chemistry), nineteen patients enrolled in the 4-week-long double-blind study were randomly assigned into two groups: a resveratrol group receiving oral 2 × 5 mg resveratrol and a control group receiving placebo. Before and after the second and fourth weeks of the trial, insulin resistance/sensitivity, creatinine-normalised ortho-tyrosine level in urine samples (as a measure of oxidative stress), incretin levels and phosphorylated protein kinase B (pAkt):protein kinase B (Akt) ratio in platelets were assessed and statistically analysed. After the fourth week, resveratrol significantly decreased insulin resistance (homeostasis model of assessment for insulin resistance) and urinary ortho-tyrosine excretion, while it increased the pAkt:Akt ratio in platelets. On the other hand, it had no effect on parameters that relate to β-cell function (i.e. homeostasis model of assessment of β-cell function). The present study shows for the first time that resveratrol improves insulin sensitivity in humans, which might be due to a resveratrol-induced decrease in oxidative stress that leads to a more efficient insulin signalling via the Akt pathway.

In order to assess nutritional adequacy, valid estimates of nutrient intake are required. One of the main errors in dietary assessment is misreporting. The objective was to review the extent, nature and determinants of misreporting in dietary assessment, how this affects reported intakes of micronutrients and how this is identified and measured, and to identify the best ways of dealing with misreporting when interpreting results. A systematic literature search was conducted for studies of misreporting of dietary intake in adults by 24 hour recalls or by estimated or weighed food records, published up to March 2008. Thirty-seven relevant studies were identified. Possible causes of misreporting were identified. Methods most used to identify misreporting were the Goldberg cut-off (46 % studies) and the doubly labelled water technique (24 % studies). The magnitude of misreporting of energy intake was similar in all three dietary assessment methods. The percentage of under-reporters was about 30 % and energy intake was underestimated by approximately 15 %. Seven papers presented usable data for micronutrient intake. Absolute intakes of Fe, Ca and vitamin C (the three micronutrients addressed in all papers) were on average 30 % lower in low-energy reporters (LER) than that in non-LER and, although results were not consistent, there was a tendency for micronutrient density to be higher in LER. Excluding underreporters or using energy adjustment methods for micronutrient intakes is discussed. Residual method of energy adjustment seems to be a good tool for practice to decrease an influence of misreporting when interpreting results of studies based on food records and 24 hour recalls.

Lipopolysaccharide (LPS) may play an important role in chronic diseases through the activation of inflammatory responses. The type of diet consumed is of major concern for the prevention and treatment of these diseases. Evidence from animal and human studies has shown that LPS can diffuse from the gut to the circulatory system in response to the intake of high amounts of fat. The method by which LPS move into the circulatory system is either through direct diffusion due to intestinal paracellular permeability or through absorption by enterocytes during chylomicron secretion. Considering the impact of metabolic diseases on public health and the association between these diseases and the levels of LPS in the circulatory system, this review will mainly discuss the current knowledge about high-fat diets and subclinical inflammation. It will also describe the new evidence that correlates gut microbiota, intestinal permeability and alkaline phosphatase activity with increased blood LPS levels and the biological effects of this increase, such as insulin resistance. Although the majority of the studies published so far have assessed the effects of dietary fat, additional studies are necessary to deepen the understanding of how the amount, the quality and the structure of the fat may affect endotoxaemia. The potential of food combinations to reduce the negative effects of fat intake should also be considered in future studies. In these studies, the effects of flavonoids, prebiotics and probiotics on endotoxaemia should be investigated. Thus, it is essential to identify dietetic strategies capable of minimising endotoxaemia and its postprandial inflammatory effects.