Inflammatory bowel diseases (IBD) are chronically relapsing inflammatory disorders of the intestine. Although some therapeutic agents, including steroids, are available for the treatment of IBD, these agents have limited use. Therefore, dietary supplements have emerged as possible interventions for IBD. Japanese honeysuckle flower, the flower of Lonicera japonica, is a well-known dietary supplement and has been used to prevent or treat various inflammatory diseases. In the present study, we investigated the effects of L. japonica on experimental murine colitis. Colitis was induced by 5 % dextran sulphate sodium (DSS) in Balb/c mice. The water extract of L. japonica (LJE) at doses of 20, 100 or 500 mg/kg was orally administered to mice twice per day for 7 d. Body weight, colon length and a histological damage score were assessed to determine the effects on colitis. Cytokine profiles were assessed to examine the effects on helper T (Th) cell-related immunological responses. In addition, CD4+CD25+Foxp3+T cells were analysed in vivo and in vitro for investigating the effects on regulatory T (Treg) cells. LJE showed dose-dependent inhibitory effects against colon shortening, weight loss and histological damage. LJE down-regulated IL-1β, TNF-α, interferon-γ, IL-6, IL-12 and IL-17. However, LJE did not show any significant effects on IL-10, IL-23, transforming growth factor-β1 and Treg cell populations. In conclusion, LJE showed protective effects against DSS-induced colitis via the Th1/Th17 pathway and not via Treg cell-related mechanisms.

Vitamin A supplementation (VAS) at birth was not associated with improved survival in a randomised, placebo-controlled trial in Guinea-Bissau. However, a negative sex-differential effect, which became evident after diphtheria–tetanus–pertussis (DTP) vaccination, was noted; among girls who had received DTP, VAS at birth was associated with two-fold higher mortality than placebo. The objective of the present study was to investigate the immunological effects of VAS at birth within a subgroup of participants in the randomised trial. Guided by the mortality results, we further explored whether VAS had a differential effect according to sex and DTP status. At 6 weeks after randomisation and supplementation, we measured differential leucocyte counts and TNF-α, interferon-γ, IL-10, IL-13 and IL-5 production in a whole-blood culture assay. A total of 471 children were included. VAS compared with placebo at birth was associated with a higher proportion of monocytes (relative risk ratio 1·26, 95 % CI 1·07, 1·49, P= 0·04), while spontaneous TNF-α production was lower in the VAS group (geometric mean ratio 0·54, 95 % CI, 0·37, 0·78, P= 0·001). Stratified analysis showed that VAS was associated with lower TNF-α and IL-10 production for girls without DTP and boys with DTP, resulting in significant three-way interactions between VAS, sex and DTP vaccination status (P= 0·03 and P= 0·04, respectively) for spontaneous TNF-α and IL-10 production. The results substantiate the potential role of VAS as an immunomodulatory intervention, which has different effects depending on concomitant health interventions and the sex of the recipient.

Previously, we showed that mice fed white button mushrooms (WBM) had enhanced immune functions known to help the body's antiviral defence. In the present study, we tested whether WBM conferred protection against viral infection. Young (4-month-old) and old (22-month-old) C57BL/6 mice were fed a diet containing 0, 2 or 10 % WBM powder for 8 weeks. Mice were then infected with influenza Puerto Rico/8/34 (H1N1), and killed at day 0 (uninfected), 2, 5 or 7 post-infection. The primary outcomes of the study were viral titre and body weight. Secondary outcomes were natural killer (NK) cell activity, lymphocyte proliferation and cytokine production. The results showed that WBM did not affect viral titre, nor did it prevent infection-induced weight loss. WBM supplementation was found to enhance NK cell activity in old mice and to increase interferon (IFN)-γ production in young and old mice under naive (uninfected) conditions, but it had no such effect after infection. The lack of a mushroom supplementation effect on NK activity and concanavalin A-stimulated IFN-γ production after infection may explain the immune system's failure to reduce viral load and weight loss in mice after influenza infection. WBM supplementation, however, did induce changes in other aspects of the immune response: it significantly increased the production of T-helper type 2 cytokines IL-4 and IL-10 in uninfected mice and pro-inflammatory cytokines IL-1β and TNF-α in infected mice. These mushroom-induced systemic changes, however, were not adequate to confer a protective effect against influenza infection.

Green tea (Camellia sinensis) catechin profiles in plasma and urine following single dosing and regular ingestion of green tea are not clear. We performed a placebo-controlled intervention study with sixteen healthy volunteers to determine changes in total and free catechins after a single dose and following 1 week of twice-daily green tea. Blood and urine samples were collected before (fasting) and after (60 and 120 min for blood; 90 and 180 min for urine) drinking 200 ml of 1·5 % (w/v) green tea or water (n 8 each), and fasting samples were again collected after 7 d of 150 ml of 1 % (w/v) supplemental green tea or water twice daily. After a 4-week washout, subjects were crossed onto the other treatment and procedures repeated. Plasma results at 1 h post-ingestion showed elevated (P< 0·05) mean epigallocatechin gallate (EGCG; 310 (sd 117) nmol/l; all in free form), epigallocatechin (EGC; 192 (sd 67) nmol/l; 30 % free) and epicatechin gallate (ECG; 134 (sd 51) nmol/l; 75 % free). Fasting plasma after 7 d of regular intake showed increased (P< 0·05) EGCG (80 v. 15 nmol/l at baseline) and ECG (120 v. 40 nmol/l), with ≥ 90 % of both in their conjugated forms. Total EGC was < 10 nmol/l. Post-ingestion conjugation and renal loss of EGC and epicatechin were rapid and high, but were negligible for EGCG and ECG. In the green tea consumed, the content was EGCG >EGC >ECG, and the acute plasma response mirrored this. However, after chronic consumption there was almost no EGC found in fasting plasma, some EGCG was present, but a rather high level of ECG was maintained.

The number of people with asthma has dramatically increased over the past few decades and the cost of care is more than $11·3 billion per year. The use of steroids is the major treatment to control asthma symptoms, but the side effects are often devastating. Seeking new drugs or new strategies to reduce the dose of steroid taken has always been an important task. A bovine whey protein extract (WPE), which is enriched in transforming growth factor-β (TGF-β), has been demonstrated to have the potential for reducing symptoms associated with mild-to-moderate T-helper cell type 1-mediated psoriasis in human subjects. However, whether WPE also has potential for inhibiting T-helper cell type 2 (Th2)-mediated disease remains unclear. In the present study, using a murine asthma model, we found that sensitised mice fed WPE daily, before they were challenged, resulted in reducing airway inflammation, serum ovalbumin-specific IgE, Th2-related cytokine production and airway hyperresponsiveness. Increase in the regulatory T cell (Treg) population in vitro and in vivo was observed when treated with WPE. According to the results from the TGF-β-blocking antibody study, we suggest that TGF-β is the main component that endows WPE with the potential to reduce the generation of Treg. Thus, the present data suggest that WPE has the potential to alleviate the symptoms of asthma by inducing the generation of Treg. Therefore, regular administration of WPE might be potentially beneficial for patients with asthma.

Dietary assessment is strongly affected by misreporting (both under- and over-reporting), which results in measurement error. Knowledge about misreporting is essential to correctly interpret potentially biased associations between diet and health outcomes. In young children, dietary data mainly rely on proxy respondents but little is known about determinants of misreporting here. The present analysis was conducted within the framework of the multi-centre IDEFICS (Identification and prevention of dietary- and lifestyle-induced health effects in children and infants) study and is based on 6101 children aged 2–9 years with 24 h dietary recall (24-HDR) and complete covariate information. Adapted Goldberg cut-offs were applied to classify the 24-HDR as ‘over-report’, ‘plausible report’ or ‘under-report’. Backward elimination in the course of multi-level logistic regression analyses was conducted to identify factors significantly related to under- and over-reporting. Next to characteristics of the children and parents, social factors and parental concerns/perceptions concerning their child's weight status were considered. Further selective misreporting was addressed, investigating food group intakes commonly perceived as more or less socially desirable. Proportions of under-, plausible and over-reports were 8·0, 88·6 and 3·4 %, respectively. The risk of under-reporting increased with age (OR 1·19, 95 % CI 1·05, 1·83), BMI z-score of the child (OR 1·23, 95 % CI 1·10, 1·37) and household size (OR 1·12, 95 % CI 1·01, 1·25), and was higher in low/medium income groups (OR 1·45, 95 % CI 1·13, 1·86). Over-reporting was negatively associated with BMI z-scores of the child (OR 0·78, 95 % CI 0·69, 0·88) and higher in girls (OR 1·70, 95 % CI 1·27, 2·28). Further social desirability and parental concerns/perceptions seemed to influence the reporting behaviour. Future studies should involve these determinants of misreporting when investigating diet–disease relationships in children to correct for the differential reporting bias.

Intestinal microbiota may influence human physiology and disease risk due to the role it plays in mediating appropriate immune responses to harmful and innocuous antigens. Colonisation of the intestine in early life seems particularly important as it is the main environmental stimulus for immune system maturation. This is a dynamic process, which depends on both environmental and genetic factors. The pathogenesis of inflammatory bowel disease, such as Crohn's disease, involves genetic polymorphisms (e.g. CARD15/nucleotide-binding oligomerisation domain 2) related to an excessive inflammatory response to commensal microbiota and to its unbalanced composition. Atopic diseases have also been linked to imbalances in microbiota and to related genetic factors (e.g. TLR4 and CD14 genes), although these associations are still controversial. Research into the relationship between the genetic risk of developing celiac disease (human leukocyte antigen (HLA)-DQ2/DQ8) and the early colonisation process in infants at family risk of the disease has also reported that the HLA-DQ genotype could influence staphylococcal colonisation. Future observational studies considering both host genetics and microbiota could be critical in defining the complex host–microbe interactions and the respective role each plays in inflammatory disorders.

Dietary methyl donors and their genetic determinants are associated with Crohn's disease risk. We investigated whether a methyl-deficient diet (MDD) may affect development and functions of the small intestine in rat pups from dams subjected to the MDD during gestation and lactation. At 1 month before pregnancy, adult females were fed with either a standard food or a diet without vitamin B12, folate and choline. A global wall hypotrophy was observed in the distal small bowel (MDD animals 0·30 mm v. controls 0·58 mm; P< 0·001) with increased crypt apoptosis (3·37 v. 0·4 %; P< 0·001), loss of enterocyte differentiation in the villus and a reduction in intestinal alkaline phosphatase production. Cleaved caspase-3 immunostaining (MDD animals 3·37 % v. controls 0·4 %, P< 0·001) and the Apostain labelling index showed increased crypt apoptosis (3·5 v. 1·4 %; P= 0·018). Decreased proliferation was observed in crypts of the proximal small bowel with a reduced number of minichromosome maintenance 6 (MDD animals 52·83 % v. controls 83·17 %; P= 0·048) and proliferating cell nuclear antigen-positive cells (46·25 v. 59 %; P= 0·05). This lack of enterocyte differentiation in the distal small bowel was associated with an impaired expression of β-catenin and a decreased β-catenin–E-cadherin interaction. The MDD affected the intestinal barrier in the proximal small bowel by decreasing Paneth cell number after immunostaining for lysosyme (MDD animals 8·66 % v. controls 21·66 %) and by reducing goblet cell number and mucus production after immunostaining for mucin-2 (crypts 8·66 v. 15·33 %; villus 7 v. 17 %). The MDD has dual effects on the small intestine by producing dramatic effects on enterocyte differentiation and barrier function in rats.

Epidemiological studies indicate that diets rich in fruits and vegetables (F&V) are protective against CVD. Puréed F&V products retain many beneficial components, including flavonoids, carotenoids, vitamin C and dietary fibres. The present study aimed to establish the physiological effects of acute ingestion of a F&V purée-based drink (FVPD) on vasodilation, antioxidant status, phytochemical bioavailability and other CVD risk factors. A total of twenty-four subjects, aged 30–70 years, completed the randomised, single-blind, controlled, crossover test meal study. Subjects consumed 400 ml of the FVPD, or a fruit-flavoured sugar-matched control, after following a low-flavonoid diet for 5 d. Blood and urine samples were collected throughout the study day, and vascular reactivity was assessed at 90 min intervals using laser Doppler iontophoresis. The FVPD significantly increased plasma vitamin C (P= 0·002) and total nitrate/nitrite (P= 0·001) concentrations. There was a near significant time by treatment effect on ex vivo LDL oxidation (P= 0·068), with a longer lag phase after consuming the FVPD. During the 6 h after juice consumption, the antioxidant capacity of plasma increased significantly (P= 0·003) and there was a simultaneous increase in plasma and urinary phenolic metabolites (P< 0·05). There were significantly lower glucose and insulin peaks after ingestion of the FVPD compared with control (P= 0·019 and 0·003) and a trend towards increased endothelium-dependent vasodilation following FVPD consumption (P= 0·061). Overall, FVPD consumption significantly increased plasma vitamin C and total nitrate/nitrite concentrations, with a trend towards increased endothelium-dependent vasodilation. Puréed F&V products are useful vehicles for increasing micronutrient status, plasma antioxidant capacity and in vivo NO generation, which may contribute to CVD risk reduction.

Conjugated linoleic acid (CLA) present in dairy and ruminant fat has beneficial effects on metabolic syndrome characteristics in humans and some rodent models. Production practices to increase the milk content of CLA are also substantially elevating trans-11-vaccenic acid (VA). Questions are being raised whether VA has the same beneficial actions as CLA or has adverse biological effects similar to industrially produced trans-fatty acids. The present study examined the effects of dietary supplementation of either 0 or 1·5 % (w/w) VA for 8 weeks on lipidaemia, glycaemia, blood pressure, hepatic steatosis, adipocyte size and molecular markers of inflammation and insulin signalling in fa/fa Zucker rats. Dietary supplementation of VA did not alter feed intake, weight gain, blood pressure or organ:body weight (BW) ratios, except the epididymal fat:BW ratio which was lower in the VA group compared with the control group. The total liver lipid concentration as an indicator of hepatic steatosis was not different between the groups. Likewise, there were no changes in fasting lipidaemia, glycaemia or oral glucose tolerance. Although there were no physiological differences observed between the groups, animals supplemented with VA had smaller adipocytes (approximately 7 % smaller than the controls). The VA group also had higher adipophilin and IL-10 protein levels in epididymal adipose tissue (1·7- and 1·4-fold higher than the controls, respectively); however, there were no changes observed in critical nodes of insulin signalling. The present study provides evidence that supplementation with VA, a naturally produced trans-fat, has some positive effects on adipose tissue and did not exacerbate obesity-mediated metabolic abnormalities.

The effects of a compound including the secondary metabolites of garlic, propyl thiosulphinate (PTS) and propyl thiosulphinate oxide (PTSO), on the in vitro and in vivo parameters of chicken gut immunity during experimental Eimeria acervulina infection were evaluated. In in vitro assays, the compound comprised of PTSO (67 %) and PTS (33 %) dose-dependently killed invasive E. acervulina sporozoites and stimulated higher spleen cell proliferation. Broiler chickens continuously fed from hatch with PTSO/PTS compound-supplemented diet and orally challenged with live E. acervulina oocysts had increased body weight gain, decreased faecal oocyst excretion and greater E. acervulina profilin antibody responses, compared with chickens fed a non-supplemented diet. Differential gene expression by microarray hybridisation identified 1227 transcripts whose levels were significantly altered in the intestinal lymphocytes of PTSO/PTS-fed birds compared with non-supplemented controls (552 up-regulated, 675 down-regulated). Biological pathway analysis identified the altered transcripts as belonging to the categories ‘Disease and Disorder’ and ‘Physiological System Development and Function’. In the former category, the most significant function identified was ‘Inflammatory Response’, while the most significant function in the latter category was ‘Cardiovascular System Development and Function’. This new information documents the immunologic and genomic changes that occur in chickens following PTSO/PTS dietary supplementation, which are relevant to protective immunity during avian coccidiosis.

Lutein and zeaxanthin are lipid-soluble antioxidants found within the macula region of the retina. Links have been suggested between increased levels of these carotenoids and reduced risk for age-related macular disease (ARMD). Therefore, the effect of lutein-based supplementation on retinal and visual function in people with early stages of ARMD (age-related maculopathy, ARM) was assessed using multi-focal electroretinography (mfERG), contrast sensitivity and distance visual acuity. A total of fourteen participants were randomly allocated to either receive a lutein-based oral supplement (treated group) or no supplement (non-treated group). There were eight participants aged between 56 and 81 years (65·50 (sd 9·27) years) in the treated group and six participants aged between 61 and 83 years (69·67 (sd 7·52) years) in the non-treated group. Sample sizes provided 80 % power at the 5 % significance level. Participants attended for three visits (0, 20 and 40 weeks). At 60 weeks, the treated group attended a fourth visit following 20 weeks of supplement withdrawal. No changes were seen between the treated and non-treated groups during supplementation. Although not clinically significant, mfERG ring 3 N2 latency (P= 0·041) and ring 4 P1 latency (P= 0·016) increased, and a trend for reduction of mfERG amplitudes was observed in rings 1, 3 and 4 on supplement withdrawal. The statistically significant increase in mfERG latencies and the trend for reduced mfERG amplitudes on withdrawal are encouraging and may suggest a potentially beneficial effect of lutein-based supplementation in ARM-affected eyes.

Pb is released from bone stores during pregnancy, which constitutes a period of increased bone resorption. A high Na intake has been found to be negatively associated with Ca and adversely associated with bone metabolism. It is possible that a high Na intake during pregnancy increases the blood Pb concentration; however, no previous study has reported on the relationship between Na intake and blood Pb concentration. We thus have investigated this relationship between Na intake and blood Pb concentrations, and examined whether this relationship differs with Ca intake in pregnant Korean women. Blood Pb concentrations were analysed in 1090 pregnant women at mid-pregnancy. Dietary intakes during mid-pregnancy were estimated by a 24 h recall method covering the use of dietary supplements. Blood Pb concentrations in whole-blood samples were analysed using graphite furnace atomic absorption spectrophotometry. Multiple regression analysis performed after adjustment for covariates revealed that maternal Na intake was positively associated with blood Pb concentration during pregnancy, but only when Ca intake was below the estimated average requirement for pregnant Korean women (P= 0·001). The findings of the present study suggest that blood Pb concentration during pregnancy could be minimised by dietary recommendations that include decreased Na and increased Ca intakes.

Increased n-6 and reduced n-3 long-chain PUFA (LC-PUFA) intake in Western diets may contribute to the increased prevalence of allergic diseases. Key effector cells in allergy are mast cells (MC). The aim of the present study was to investigate the effects of n-6 v.n-3 LC-PUFA on MC phenotype. Human MC lines (LAD2 and HMC-1) were incubated for 24 h with either arachidonic acid (AA, n-6 LC-PUFA) or the n-3 LC-PUFA EPA or DHA. The effects of these three LC-PUFA on degranulation, mediator secretion and reactive oxygen species (ROS) generation were assessed. ROS, mitogen-activated protein kinase (MAPK) or NF-κB inhibitors were used to unravel signalling pathways involved in cytokine secretion. AA, EPA or DHA did not reduce IgE-mediated degranulation by LAD2 cells. However, AA increased PGD2 and TNF-α secretion by ionomycin/phorbol 12-myristate 13-acetate-stimulated HMC-1, whereas EPA and DHA more prominently inhibited IL-4 and IL-13 secretion. Suppression of IL-4 and IL-13 release by LC-PUFA correlated with reduced ROS generation. IL-4 and IL-13 release by activated HMC-1 was abrogated using ROS inhibitors. Inhibition of MAPK signalling, but not NF-κB, downstream of ROS reduced IL-13 secretion by activated HMC-1. Combined incubation of EPA or DHA with MAPK inhibitors further suppressed IL-13 secretion. In conclusion, the n-6 LC-PUFA AA enhanced pro-inflammatory mediator production by MC, while the n-3 LC-PUFA EPA as well as DHA more effectively suppressed ROS generation and IL-4 and IL-13 release. This suggests that dietary supplementation with EPA and/or DHA may alter the MC phenotype, contributing to a reduced susceptibility to develop and sustain allergic disease.

Growing evidence suggests that n-3 PUFA and their specific lipid mediators can reduce the activity of inflammatory processes. In the present study, we evaluated the effects of oral n-3 PUFA supplementation on intestinal structural changes, enterocyte proliferation and apoptosis during methotrexate (MTX)-induced intestinal damage in the rat. A total of thirty-two male rats were divided into four experimental groups: control (CONTR) rats; CONTR-n-3 PUFA rats treated with oral administration of n-3 PUFA at a dose of 300 μg/kg once per d 72 h before and 72 h following vehicle injection; MTX rats treated with a single dose of MTX; MTX-n-3 PUFA rats treated with oral n-3 PUFA following the injection of MTX. Intestinal mucosal damage, mucosal structural changes, enterocyte proliferation and enterocyte apoptosis determined 72 h following MTX injection. Real-time PCR was used to determine B-cell lymphoma 2 (Bcl2)-associated X protein (Bax) and Bcl2 mRNA expression. Western blotting was used to determine phosphorylated extracellular signal-related kinase, β-catenin, Bax and Bcl2 protein levels. MTX-n-3 PUFA rats demonstrated a greater jejunal and ileal bowel weight, greater ileal mucosal weight, greater ileal mucosal DNA and protein levels, greater villus height in the jejunum and ileum and crypt depth in the ileum, compared with MTX animals. A significant decrease in enterocyte apoptosis in the ileum of MTX-n-3 PUFA rats (v. MTX) was accompanied by decreased Bax mRNA and protein expression and increased Bcl2 mRNA levels. Thus, the treatment with oral n-3 PUFA prevented mucosal injury and improved intestinal recovery following MTX-injury in rats.

Nut consumption is associated with a reduced risk of type 2 diabetes mellitus (T2DM). The aim of the present study was to assess the effects of adding peanuts (whole or peanut butter) on first (0–240 min)- and second (240–490 min)-meal glucose metabolism and selected gut satiety hormone responses, appetite ratings and food intake in obese women with high T2DM risk. A group of fifteen women participated in a randomised cross-over clinical trial in which 42·5 g of whole peanuts without skins (WP), peanut butter (PB) or no peanuts (control) were added to a 75 g available carbohydrate-matched breakfast meal. Postprandial concentrations (0–490 min) of glucose, insulin, NEFA, glucagon-like peptide-1 (GLP-1), peptide YY (PYY), cholecystokinin (CCK), appetitive sensations and food intake were assessed after breakfast treatments and a standard lunch. Postprandial NEFA incremental AUC (IAUC) (0–240 min) and glucose IAUC (240–490 min) responses were lower for the PB breakfast compared with the control breakfast. Insulin concentrations were higher at 120 and 370 min after the PB consumption than after the control consumption. Desire-to-eat ratings were lower, while PYY, GLP-1 and CCK concentrations were higher after the PB intake compared with the control intake. WP led to similar but non-significant effects. The addition of PB to breakfast moderated postprandial glucose and NEFA concentrations, enhanced gut satiety hormone secretion and reduced the desire to eat. The greater bioaccessibility of the lipid component in PB is probably responsible for the observed incremental post-ingestive responses between the nut forms. Inclusion of PB, and probably WP, to breakfast may help to moderate glucose concentrations and appetite in obese women.

Experimental data in animals, but also observational studies in obese patients, suggest that the composition of the gut microbiota differs in obese v. lean individuals, in diabetic v. non-diabetic patients or in patients presenting other diseases associated with obesity or nutritional dysbalance, such as non-alcoholic steatohepatitis. In the present review, we will describe how changes in the gut microbiota composition and/or activity by dietary fibres with prebiotic properties, can modulate host gene expression and metabolism. We will evaluate their potential relevance in the management of obesity and related metabolic disturbances, in view of the experimental data and intervention studies published up to date.

Anthropometric data indicate that the human phenotype is changing. Today's adult is greater in stature, body mass and fat mass. Accurate measurement of body composition is necessary to maintain surveillance of obesity within the population and to evaluate associated interventions. The aim of the present study was to construct and validate generalised equations for percentage body fat (%BF) prediction from anthropometry in 1136 adult men and women. Reference values for %BF were obtained using dual-energy X-ray absorptiometry. Skinfold thickness (SF) at ten sites and girth (G) at seven sites were measured on 736 men and women aged 18–81 years (%BF 5·1–56·8 %). Quantile regression was employed to construct prediction equations from age and log-transformed SF and G measures. These equations were then cross-validated on a cohort of 400 subjects of similar age and fatness. The following generalised equations were found to most accurately predict %BF: $Men:\,(age\times 0\cdot 1) + (logtricepsSF\times 7\cdot 6) + (logmidaxillaSF\times 8\cdot 8) + (logsuprspinaleSF\times 11\cdot 9) - 11\cdot 3$$$ (standard error of the estimate: 2·5 %, 95 % limits of agreement: − 4·8, +4·9) $Women:\,(age\times 0\cdot 1) + (logabdominalG\times 39\cdot 4) + (logmidaxillaSF\times 4\cdot 9) + (logbicepsSF\times 11\cdot 0) + (logmedialcalfSF\times 9\cdot 1) - 73\cdot 5$$$ (standard error of the estimate: 3·0 %, 95 % limits of agreement: − 5·7, + 5·9) These generalised anthropometric equations accurately predict %BF and are suitable for the measurement of %BF in adult men and women of varying levels of fatness across the lifespan.

Fenugreek seed has been shown to affect the intestinal microbiota and immunological responses in animals. A feeding trial with male castrated piglets was performed over 28 d without or with the addition of 1·5 g fenugreek seeds/kg complete diet in ten and eleven piglets, weaned at 21 d. In the intestinal tract, pH, lactate and SCFA were measured as major bacterial metabolites. Immune cell phenotypes, phagocytic activity and lymphocyte proliferation after stimulation with pokeweed mitogen, concanavalin A and phytohaemagglutinin M were measured by flow cytometry. Health status and performance of the piglets were not affected by fenugreek. The pH in the caecum and colon were reduced compared with the control (P< 0·05). Higher concentrations of l-lactic acid were recorded in the small-intestinal digesta (average concentrations from the duodenum, jejunum and ileum; P< 0·05), while the concentrations of SCFA remained unchanged except an increase in n-butyric acid in colon contents (P< 0·05). The piglets fed the fenugreek diet had higher Lactobacillus and clostridium cluster I concentrations and lower Escherichia, Hafnia and Shigella concentrations in the small intestine. The addition of fenugreek increased the relative concentration of the γδ T-cell population (TCR1+CD8α−) in the blood with a simultaneous reduction of antigen-presenting cells (MHCII+CD5−) (P< 0·05). Proliferation rate and phagocytosis activity of monocytes were not affected by the additive. In conclusion, fenugreek seeds might be interesting as a feed ingredient for young piglets due to their effects on the intestinal microbiota and immunological variables. The impact on performance and animal health has to be further evaluated.

Intake of dairy fat has long been considered as a risk factor for CVD. Pasture and dietary lipid supplementation have been reported to be reliable strategies in ruminant nutrition, in order to increase the content of α-linolenic acid (ALA), conjugated linoleic acid (CLA) and vaccenic acid (VA), and decrease SFA in milk fat. In the present study, we aimed at verifying whether consumption of a sheep cheese, naturally enriched in ALA, CLA and VA, would modify the plasma lipid and endocannabinoid profiles in mildly hypercholesterolaemic subjects. A total of forty-two adult volunteers (nineteen males and twenty-three females) with diagnosed mildly hypercholesterolaemia (total cholesterol 5·68–7·49 mmol/l) were randomly assigned to eat 90 g/d of a control or enriched cheese for 3 weeks, with a cross-over after 3 weeks of washout. Plasma lipids, endocannabinoids, adipokines and inflammatory markers were measured. The intake of enriched cheese significantly increased the plasma concentrations of CLA, VA, the n-3 fatty acids ALA and EPA, and more remarkably decreased that of the endocannabinoid anandamide. LDL-cholesterol decreased significantly (7 %). No changes were detected in the levels of inflammatory markers; however, a significant correlation was found between the plasma levels of anandamide and leptin. The control cheese modified none of the parameters measured. The results obtained do not support the view that intake of dairy fat is detrimental to hypercholesterolaemic subjects. Indeed, they show that a naturally enriched cheese possesses beneficial properties, since it ameliorates the plasma lipid profile, and more remarkably reduces endocannabinoid biosynthesis.