In mammals, (n-3) PUFA and conjugated linoleic acids (CLA) act as activators of PPARα and alter nuclear concentrations of sterol regulatory element-binding proteins (SREBP) in the liver, and thereby influence hepatic lipid catabolism and synthesis. In this study, we investigated the hypothesis that (n-3) PUFA and CLA exert similar effects in the liver of laying hens. Thirty hens (64 weeks old) were fed diets containing 30 g/kg of sunflower oil (control), fish oil (salmon oil) or CLA in TAG form (containing predominantly cis-9, trans-11 CLA and trans-10, cis-12 CLA) for 5 weeks. Hens fed fish oil had a higher expression of some PPARα target genes and a lower nuclear concentration of SREBP-2 in the liver and lower concentrations of cholesterol and TAG in plasma than control hens. Nuclear concentration of SREBP-1 and its target genes involved in lipogenesis were not altered in hens fed fish oil. Hens fed CLA had increased concentrations of TAG and cholesterol in the liver. However, their mRNA levels of PPARα target genes and nuclear concentrations of SREBP-1 and SREBP-2 as well as mRNA levels of their target genes in the liver were largely unchanged compared to control hens. The results of this study suggest that (n-3) PUFA cause a moderate activation of PPARα and lower cholesterol synthesis but do not impair fatty acid synthesis in the liver of laying hens. CLA lead to an accumulation of TAG and cholesterol in the liver of hens by mechanisms to be elucidated in further studies.

Fermentation products, SCFA, particularly butyrate, are considered a sign of ‘good’ bowel health but the influence of bacterial population composition and diet on inter-individual difference in metabolites and colonic health is poorly understood. Faecal specimens were collected weekly from eight healthy human volunteers over 12 weeks. Dietary intake was self-reported and ten macronutrient factors were analysed at selected weekly periods. Faecal weight, pH and moisture were recorded, and SCFA concentrations were measured in all samples. From each specimen, DNA was prepared and eubacterial 16S rRNA gene PCR performed. Bacterial population profiles were captured by denaturing gradient gel electrophoresis (DGGE) of PCR products, and multivariate statistical analysis was performed. Faecal weight, pH and moisture varied widely within and between individuals. Average total SCFA concentrations over 12 weeks ranged from 36·9 to 144·4 mmol/kg in 48 h specimens and faecal butyrate concentrations ranged from 1·8 to 48·5 mmol/kg. Two individuals with butyrate concentrations below 10 mmol/kg were considered to be ‘low butyrate types’ and may represent an at-risk population for bowel health. Dietary fat, sugar and carbohydrate showed weak correlation with SCFA (R − 0·612, P = 0·015; R 0·607, P = 0·016; R 0·610, P = 0·016, respectively) and butyrate concentrations (R − 0·593, P = 0·02; R 0·504, P = 0·054; R 0·528, P = 0·043, respectively). Multivariate analysis of DGGE bacterial profiles demonstrated concise and repeated grouping of intra-individual samples, but these were combined with distinct inter-individual differences (analysis of similarities P < 0·001, R ≥ 0·99) The exact relationship of these SCFA values to the overall bacterial profiles and SCFA-producer bacterial groups was not direct nor linear.

The purpose of the present study was to evaluate the effect of Ramadan fasting on insulin sensitivity in subjects with the metabolic syndrome. Males (n 55; age 34·1 (sd 8·9) years) with the metabolic syndrome were studied. Blood pressure, waist circumference, body weight, HDL-cholesterol (HDL-C), TAG, fasting plasma glucose (FPG), fasting blood insulin and insulin resistance indices (quantitative insulin sensitivity check index (QUICKI), homeostasis model assessment of insulin resistance (HOMA-IR) and reciprocal index of HOMA-IR (1/HOMA-IR)) were evaluated before and after 30 d of Ramadan fasting (two meals at 12 h intervals). The dietary intake was estimated by 24 h recall before and after fasting. The total daily energy intake was decreased by 234·6 (sd 88·2) kJ/d in the fasting period (P = 0·005). 1/HOMA-IR, QUICKI and HDL-C were significantly increased (P = 0·005, P = 0·001 and P = 0·004) and FPG significantly decreased (P < 0·005) after fasting. Simple linear regression analysis demonstrated that HOMA-IR, 1/HOMA-IR and QUICKI were related to waist circumference after intervention (r 0·458, P < 0·001; r − 0·396, P < 0·05; r − 0·342, P < 0·05). In conclusion, the present study showed that the combined change in the number and timing of meals and portioning of the entire intake into only two meals per d may increase insulin sensitivity in subjects with the metabolic syndrome even when the decrease in energy consumption is minimal.

The calculation of body composition using bioelectrical impedance analysis in sick and hospitalized patients is hampered due to altered hydration state. We wanted to investigate how disease-related malnutrition assessed by the Subjective Global Assessment (SGA) is reflected in the bioelectrical impedance vector analysis. Patients with benign gastrointestinal disease (n 242) were entered in the study. Nutritional status was assessed by SGA. Arm muscle and fat area were estimated by anthropometry, muscle function was determined by hand grip strength. Whole body impedance measurements were made at 50 kHz. Ninety-eight patients were considered well nourished (SGA A), ninety-four were classified moderately malnourished (SGA B) and fifty patients were classified severely malnourished (SGA C) according to the SGA. The mean vector was significantly displaced between SGA C and SGA A and B, showing comparable resistance with a significantly reduced reactance, indicating comparable hydration but loss of dielectrical mass of soft tissues. This distinctive vector migration was not seen when studying the patients grouped according to BMI. In conclusion, disease-related malnutrition as assessed by the SGA is associated with a distinctive bioelectrical vector migration, implying that abnormal tissue structure and not reduced body mass only occurs in disease-related malnutrition. These disturbances are not seen in underweight according to BMI. Bioelectrical impedance vector analysis appears to be an attractive tool to identify disease-related malnutrition and to monitor nutritional intervention.

The usefulness of the glycaemic index (GI) of a food for practical advice for individuals with diabetes or the general population depends on its reliability, as estimated by intra-class coefficient (ICC), a measure having values between 0 and 1, with values closer to 1 indicating better reliability. We aimed to estimate the ICC of the postprandial blood glucose response to glucose and white bread, instant mashed potato and chickpeas using the incremental area under the curve (iAUC) and the GI of these foods. The iAUC values were determined in twenty healthy individuals on three and four occasions for white bread and glucose, respectively, and for potato and chickpeas on a single occasion. The ICC of the iAUC for white bread and glucose were 0·50 (95 % CI 0·27, 0·73) and 0·49 (95 % CI 0·22, 0·75), respectively. The mean GI of white bread was 81 (95 % CI 74, 90) with a reliability of 0·27 indicating substantial within-person variability. The GI of mashed potato and chickpeas were 87 (95 % CI 76, 101) and 28 (95 % CI 22, 37) respectively with ICC of 0·02 and 0·40.The ICC of the iAUC were moderate and those of the GI fair or poor, indicating the heterogeneous nature of individuals' responses. The unpredictability of individual responses even if they are the result of day-to-day variation places limitations on the clinical usefulness of GI. If the very different GI of potato and chickpeas are estimates of an individual's every-day response to different foods, then the GI of foods may provide an indication of the GI of a long-term diet.

Felinine is a branched-chain sulfur amino acid present in the urine of certain Felidae, including domestic cats. The objective of the present study was to determine if additional cystine and/or dietary N would increase felinine and N-acetylfelinine excretion by intact male cats fed a low-protein (LP) diet. Feeding five adult intact male cats an LP diet (18·8 % of metabolisable energy (ME) as protein) v. a high-protein diet (38·6 % of ME as protein) resulted in a trend (P = 0·08) for decreased urinary felinine and no change in N-acetylfelinine excretion. In a 23 d study, when the LP diet was supplemented with l-cystine at 9·3 g/kg DM, urinary felinine:creatinine ratio showed a linear two-fold (121 %) increase (P < 0·01) from 0·24 (sem 0·05) to 0·53 (sem 0·13) after 10 d. Subsequent feeding of the LP diet resulted in a decrease in felinine excretion to base levels. Plasma γ-glutamylfelinylglycine concentrations were consistent with the excretion of felinine. Supplementation of the LP diet with l-cystine (9·3 g/kg DM), dispensable amino acids and arginine to a second group (n 5) also resulted in a significant (P < 0·01) but smaller (+72 %) increase in the daily felinine:creatinine ratio (0·25 (sem 0·04) to 0·43 (sem 0·05)). The degree of felinine N-acetylation within groups was unaffected by dietary addition and withdrawal of amino acids. The results indicate that felinine synthesis is regulated by cystine availability, and that arginine may be physiologically important in decreasing felinine biosynthesis in intact male cats.

The aim of the present study was to determine whether under-reporting rates vary between dietary pattern clusters. Subjects were sixty-five Brazilian women. During 3 weeks, anthropometric data were collected, total energy expenditure (TEE) was determined by the doubly labelled water method and diet was measured. Energy intake (EI) and the daily frequency of consumption per 1000 kJ of twenty-two food groups were obtained from a FFQ. These frequencies were entered into a cluster analysis procedure in order to obtain dietary patterns. Under-reporters were defined as those who did not lose more than 1 kg of body weight during the study and presented EI:TEE less than 0·82. Three dietary pattern clusters were identified and named according to their most recurrent food groups: sweet foods (SW), starchy foods (ST) and healthy (H). Subjects from the healthy cluster had the lowest mean EI:TEE (SW = 0·86, ST = 0·71 and H = 0·58; P = 0·003) and EI − TEE (SW = − 0·49 MJ, ST = − 3·20 MJ and H = − 5·08 MJ; P = 0·008). The proportion of under-reporters was 45·2 (95 % CI 35·5, 55·0) % in the SW cluster; 58·3 (95 % CI 48·6, 68·0) % in the ST cluster and 70·0 (95 % CI 61·0, 79) % in the H cluster (P = 0·34). Thus, in Brazilian women, under-reporting of EI is not uniformly distributed among dietary pattern clusters and tends to be more severe among subjects from the healthy cluster. This cluster is more consistent with both dietary guidelines and with what lay individuals usually consider ‘healthy eating’.

Epidemiological studies indicate a J-shaped relationship linking coffee consumption and cardiovascular risk, suggesting that moderate coffee consumption can be beneficial. Platelet aggregation is of critical importance in thrombotic events, and platelets play a major role in the aetiology of several CVD. The aim of this study was to evaluate the effect of coffee drinking on platelet aggregation ex vivo, using caffeine as control. A crossover study was performed on ten healthy subjects. In two different sessions, subjects drank 200 ml coffee, containing 180 mg caffeine, or a capsule of caffeine (180 mg) with 200 ml water. Platelets were separated from plasma at baseline and 30 and 60 min after coffee drinking. Platelet aggregation was induced with three different agonists: collagen, arachidonic acid and ADP. Coffee drinking inhibited collagen (P < 0·05 from baseline at time 30 min) and arachidonic acid (P < 0·05 from baseline at time 60 min) induced platelet aggregation. Caffeine intake did not affect platelet aggregation induced by the three agonists. Coffee consumption induced a significant increase of platelet phenolic acids (likely present as glucuronate and sulphate derivatives), caffeic acid, the principal phenolic acid in coffee, raising from 0·3 (sem 0·1) to 2·4 (sem 0·6) ng/mg (P < 0·01). Caffeine was not detectable in platelets. Coffee drinking decreases platelet aggregation, and induces a significant increase in phenolic acid platelet concentration. The antiplatelet effect of coffee is independent from caffeine and could be a result of the interaction of coffee phenolic acids with the intracellular signalling network leading to platelet aggregation.

The impact of apo E phenotypes on applicability of relative cholesterol synthesis (lathosterol:cholesterol) and absorption (ratios of cholestanol, campesterol and sitosterol to cholesterol) during diets of various cholesterol and fat content is unclear. We examined and compared with each other both relative and absolute synthesis and absorption among twenty-nine men, of whom eight, nine and twelve had apo E phenotypes 2 (2/2, 2/3, 2/4), 3 (3/3) and 4 (3/4, 4/4), respectively. Serum lipids, lipoproteins, sterols and cholesterol metabolism were examined on four subsequent diets: high-cholesterol high-fat (home diet; HD), low-cholesterol low-fat (LCLF), high-cholesterol low-fat (HCLF) and low-cholesterol high-fat (LCHF). LDL-cholesterol (LDL-C) level was about 40 % lower (P < 0·05) in apo E2 than apo E3 and E4 groups irrespective of dietary fat and cholesterol. Serum proportions of phytosterols were determined apo E-dependently on LCLF and HCLF, and those of lathosterol, cholestanol and campesterol were increased in apo E2 and E3 groups (P < 0·05 for each v. HD). Serum proportion of sitosterol reflected almost consistently apo E phenotype (r range+0·308 to+0·383; P range 0·214–0·011). Relative cholesterol synthesis and absorption reflected respective absolute values during each diet in the apo E4 group (r range+0·713 to+0·893; P < 0·05 for each), but only during HD (r+0·594; P = 0·015) in the apo E2+E3 group. The consumption of a high amount of fat did not interfere with cholesterol metabolism or serum levels of LDL-C differently in apo E phenotypes. Surrogate sterol markers of cholesterol metabolism reflected absolute ones (especially in the apo E4 group) and apo E phenotypes despite variable amounts of dietary cholesterol and fat.

Diet composition influences net endogenous acid production (NEAP), which may affect bone health. No studies are available to relate dietary estimate of NEAP to bone health in Chinese adolescents. This study examined the association of dietary estimates of NEAP with bone mineral status in Hong Kong Chinese adolescents. Baseline data on 171 boys and 180 girls aged 10–12 years from the Hong Kong Adolescent Bone Health Cohort Study were presented. Weight, height, Tanner stage and dietary intakes by FFQ were collected. NEAP was estimated from diet using Frassetto's method. Bone area (BA), bone mineral content (BMC) and bone mineral apparent density (BMAD) of total hip, lumbar (L1–L4) spine and whole body were estimated by dual-energy X-ray absorptiometry (DXA). No significant association was observed between BMC or BMAD and energy-adjusted NEAP or other nutrients. BA was significantly and positively associated with BMC at all sites in both sexes. Weight was significantly and positively associated with BMC in hip and spine in both sexes. Height was negatively correlated with hip BMC for boys and whole body BMC for girls. Pubertal stage was significantly and positively associated with BMC in all sites in both sexes. Weight and height contributed most of the variability in BMAD at different sites. The results suggest that anthropometric characteristics and pubertal stage are more influential than dietary NEAP in determining bone mineral status of Hong Kong Chinese adolescents. However, the methodological weaknesses regarding the use of DXA and FFQ in the present sample require attention.

Recent work shows that increased meal frequency reduces ghrelin responses in sheep. Human research suggests there is an interaction between insulin and ghrelin. The effect of meal frequency on this interaction is unknown. Therefore, we investigated the effect of feeding frequency on insulin and ghrelin responses in human subjects. Five healthy male volunteers were recruited from the general population: age 24 (sem 2) years, body mass 75·7 (sem 3·2) kg and BMI 23·8 (sem 0·8) kg/m2. Volunteers underwent three 8-h feeding regimens: fasting (FAST); low-frequency (two) meal ingestion (LOFREQMEAL); high-frequency (twelve) meal ingestion (HIFREQMEAL). Meals were equi-energetic within trials, consisting of 64 % carbohydrate, 23 % fat and 13 % protein. Total energy intake was equal between feeding trials. Total area under the curve for serum insulin and plasma ghrelin responses did not differ between trials (P>0·05), although the hormonal response patterns to the two meal feeding regimens were different. An inverse relationship was found between serum insulin and plasma ghrelin during the FAST and LOFREQMEAL trials (P < 0·05); and, in the postprandial period, there was a time delay between insulin responses and successive ghrelin responses. This relationship was not observed during the HIFREQMEAL trial (P>0·05). This study provides further evidence that the postprandial fall in ghrelin might be due, at least partially, to the rise in insulin and that high-frequency feeding may disrupt this relationship.

The study was conducted to determine the effectiveness of a modified Mini Nutritional Assessment (MNA) for assessing the nutritional status and predicting follow-up mortality of institutionalized elderly Taiwanese. The study was conducted in a large long-term care centre in central Taiwan. Trained interviewers assisted by the caregivers elicited sociodemographic data, healthcare and disease history, and answers to the MNA screen from each subject. One researcher performed all subjects' anthropometric measurements. Plasma albumin and cholesterol concentrations were determined. Results showed that the MNA without BMI, modified according to population-specific mid-arm circumference and calf circumference cut-points, effectively predicted the nutritional risk status of the elderly regardless of cognitive status. Substituting caregiver's assessments for self-viewed nutrition and health status (questions O and P of MNA) improved the predicting power of the tool in cognition-normal subjects. Results showed that 21·9 % of the elderly were malnourished, 59·2 % were at risk of malnutrition and 18·9 % were normal according to self-assessment whereas 14·2 % were malnourished, 59·2 % were at risk of malnutrition, and 26·6 % were normal according to caregiver's evaluation. The tool was also effective in predicting 12- and 6-month follow-up mortality in cognition-normal and cognition-impaired elderly, respectively. Results indicate that a population-specific MNA can effectively predict the nutritional status and 6-month follow-up mortality of elderly Taiwanese regardless of cognitive condition. Easier and wider application of the tool will enable early detection of emerging nutritional problems and timely intervention to prevent the development of severe malnutrition in the elderly.

Previous studies with folate/methyl-deficient rat models proposed the role of folate deficiency in hepatocarcinogenesis and tumour progression. We investigated the relationship between folate status and tumour progression in patients with hepatocellular carcinoma (HCC). Ninety HCC patients (age 62 (sd 10) years) recruited through the Department of Internal Medicine, Chi-Mei Hospital, participated in this cross-sectional study. According to the clinical criteria, 44 % showed marginal folate deficiency (serum folate 7–14 nmol/l; folate intake 278 (sd 212) μg/d), and 16 % were folate deficient ( < 7 nmol/l; 207 (sd 113) μg/d). Serum folate showed inverse correlations with three elements of tumour progression: tumour size (r − 0·29; P = 0·005), tumour multiplicity (r − 0·24; P = 0·018) and metastasis (r − 0·39; P = 0·0001). When HCC progression was categorised into stages I to IV, serum folate decreased as HCC stage progressed (stage I, 24·5 (sd 11·5); stage IV, 10·3 (sd 3·3) nmol/l; P = 0·032). After adjustment for age, sex, lifestyle and dietary factors, patients with low blood folate status (serum folate < 14 nmol/l) had increased risks for advanced tumour progression in large tumours (OR 7·1 (95 % CI 2·27, 21·9); P = 0·0007), tumour multiplicity (OR 3·2 (95 % CI 1·07, 3·51); P = 0·004) and metastasis (OR 4·5 (95 % CI 1·11, 18·4); P = 0·03) relative to those with normal folate status. Further controlling for liver injury, tumour proliferation and tumour stage, however, negated the effect of folate on advanced tumour progression. The data thus suggest that low blood folate status could be a risk factor for tumour progression, which is modulated by clinical lesions present in HCC patients. Future studies with larger sample sizes are warranted to explore the joint effects of low folate and hepatic lesions in human HCC malignancy.

This study assesses the stability of dietary patterns obtained using principal components analysis (PCA) through early to mid-childhood. Dietary data were collected from children in the Avon Longitudinal Study of Pregnancy and Childhood (ALSPAC). Frequency of consumption of a range of food items was recorded by mothers using self-completion postal questionnaires when their children were 3, 4, 7 and 9 years of age. Dietary patterns were identified using PCA and component scores were calculated at each time-point. In total 6177 children had data available at all four time-points. Three patterns were consistently seen across time: the ‘processed’, ‘traditional’ and ‘health conscious’ patterns. At 3 years an additional ‘snack’ pattern was obtained and at 9 years the ‘health conscious’ pattern was slightly modified (meat products were negatively associated). High correlations were evident for all three scores between each pair of time-points. The widest limits of agreement were seen for all pairings between the 3 and 9 years data, whilst the narrowest were seen between the 4 and 7 years data. A reasonable level of agreement was seen with the categorised component scores from each time-point of data (κ ranging from 0·28 to 0·47). Virtually identical dietary patterns were obtained at the ages of 4 and 7; however, periods of change were apparent between the ages of 3 and 4 and the ages of 7 and 9. It is important to make regular dietary assessments during childhood in order to assess accurately the effects of diet on future health outcomes.

This study aimed to investigate the clinical usefulness of an anthropometrically based method for estimating leg lean volume (LLV) in patients with chronic obstructive pulmonary disease (COPD) who presented or not with nutritional depletion. We prospectively evaluated a group of forty-eight patients (thirty-eight males) with moderate to severe COPD (Global Initiative for Chronic Obstructive Lung disease stages II–IV) who underwent a 6 min walking test and knee isokinetic dynamometry. Leg lean mass (muscle mass plus bone) was determined by dual-energy X-ray absorptiometry (DEXA) with derivation of its respective volume: these values were compared with those obtained by the truncated cones method first described by Jones and Pearson in 1969. As expected, depleted patients (n 19) had reduced exercise capacity and impaired muscle performance as compared to non-depleted subjects (P < 0·01). The mean bias of the LLV differences between anthropometry and DEXA were 0·40 litre (95 % CI − 0·59, 1·39) and 0·50 litre (95 % CI − 1·08, 2·08) for depleted and non-depleted patients, respectively. Anthropometrically and DEXA-based estimates correlated similarly with muscle functional attributes. A ROC curve analysis revealed that leg height-corrected LLV values had acceptable sensitivity and specificity to identify depleted patients (area under the curve 0·93 (range 0·86–1·00); P < 0·001). Moreover, patients with LLV ≤ 9·2 litres/m (the best cut-off value according to the ROC curve) had significantly lower exercise capacity and muscle performance than their counterparts (P < 0·05). In conclusion, an anthropometrically based method of estimating LLV (Jones and Pearson method) was shown to present with clinically acceptable accuracy and external validity in depleted and non-depleted patients with stable COPD.

We evaluated whether plant stanol esters mixed with different vegetable oil spreads improved arterial health. A total of 200 adults with serum cholesterol >5 mmol/l were randomised to consume camelina, rapeseed or sunflower oil spread with stanol (2 g/d) ester or sunflower oil spread without stanol ester (controls) for 3 months. Non-invasive ultrasound was used to measure carotid artery compliance (CAC) and brachial artery flow-mediated endothelial dependent vasodilatation (FMD) at baseline and after the intervention as markers of arterial health. Plant stanol esters reduced LDL-cholesterol by 9 % compared with controls (P < 0·001) similarly in the different treatment groups. In the combined treatment groups (n 147), CAC or FMD were not changed from controls (n 47). In a subgroup analysis, division of subjects at baseline into below and over sex-specific 50th percentiles of CAC and FMD revealed that low CAC was improved from 1·23 to 1·59 % per 10 mmHg in the treatment group (n 69), and from 1·42 to 1·47 % per 10 mmHg in controls (n 25), (P = 0·0035 between groups). Low FMD was improved from 6·9 % to 8·6 % in the treatment group (n 73) and from 6·6 % to 6·8 % in controls (n 24) (P = 0·05 between groups). In the respective high-median groups, CAC and FMD were not changed in spite of significantly lowered LDL-cholesterol. In conclusion, consumption of plant stanol ester for 3 months had no overall significant effect on arterial elasticity and endothelial function. A controlled study is needed to test whether beneficial changes are obtained in subjects with initially reduced arterial elasticity and endothelial function.

Traditional cardiovascular risk factors are associated with endothelial dysfunction. The vascular endothelium plays a key role in local vascular tone regulation and can be modulated by dietary fat. We propose to determine the chronic effect of three diets with different fat compositions on postprandial endothelial function and inflammatory biomarkers. Twenty healthy men followed three 4-week diets in a randomised cross-over design: a Western diet, rich in saturated fat (22 % SFA, 12 % MUFA and 0·4 % α-linolenic acid (ALA), all fractions are % of energy); a Mediterranean diet, rich in MUFA ( < 10 % SFA, 24 % MUFA and 0·4 % ALA); a low-fat diet enriched in ALA ( < 10 % SFA, 12 % MUFA and 2 % ALA). At the end of each dietary period all subjects underwent a postprandial study. Plasma concentrations of lipid parameters, soluble intercellular cell-adhesion molecule-1, soluble vascular cell-adhesion molecule-1 (sVCAM-1), nitrates and nitrites (NOx) and endothelial function studied by laser Doppler were examined at 0, 2, 4, 6 and 8 h. The endothelium-dependent vasodilatory response was greater 4 h after the ingestion of the MUFA-rich diet than after the SFA or ALA low-fat diets (P = 0·031). The 4 h postprandial plasma sVCAM-1 levels were lower after the MUFA meals than after the ALA low-fat diet (P = 0·043). The bioavailability of NOx was higher following the MUFA diet than after the SFA and ALA low-fat diets (P = 0·027). We found no differences in the other parameters measured. Chronic ingestion of a Mediterranean diet avoids the postprandial deterioration of endothelial function associated with Westernised diets in healthy individuals.

The serum albumin level is a widely accepted indicator of nutritional status in healthy adults and elderly individuals. However, there are few data regarding the distribution and correlates of serum albumin levels in individuals with intellectual and/or motor disabilities. We conducted a cross-sectional study at a public facility for individuals with intellectual and/or motor disabilities in Ibaraki prefecture, Japan. Health check-up data obtained in 2001 from 477 individuals with intellectual disability (286 males, average age 40·6 (sd 12·3) years; 191 females, average age 45·1 (sd 11·6) years) were retrospectively reviewed. With the exception of men with cerebral palsy, the serum albumin level was nearly normally distributed. The mean was 44 (sd 3·6) g/l for males and 44 (sd 3·6) g/l for females with intellectual disability, 43 (sd 3·2) g/l in males and 44 (sd 2·6) g/l for females with cerebral palsy, 41 (sd 2·7) g/l for males and 42 (sd 3·7) g/l for females with Down's syndrome, and 42 (sd 4·5) g/l for males and 41 (sd 3·2) g/l for females with severe motor and intellectual disabilities. Only six of 474 individuals (1·3 %) had a serum albumin ≤ 35 g/l. Low serum albumin was related to age, use of anticonvulsants and/or major tranquilisers, use of other medications, high C-reactive protein (CRP), high zinc sulfate turbidity test (ZTT), low serum Hb and low serum Fe among men; among women, high CRP and high ZTT were related to low serum albumin. The present study found an unexpectedly low incidence of low serum albumin among institutionalised individuals with intellectual and/or motor disabilities. Low serum albumin was associated with age, medications and inflammation in men, as well as inflammation in women.

Specific carbohydrates, i.e. prebiotics such as fructo-oligosaccharide (FOS), are not digested in the small intestine but fermented in the colon. Besides beneficial health effects of an enhanced bifidobacteria population, intestinal gas production resulting from fermentation can induce abdominal symptoms. Partial replacement with slowly fermented acacia gum may attenuate side effects. The aim was to compare the effects of FOS with those of a prebiotic mixture (50 % FOS and 50 % acacia gum; BLEND) and a rapidly absorbed carbohydrate (maltodextrin) on general intestinal wellbeing, abdominal comfort and anorectal sensory function. Twenty volunteers (eight male and twelve female; age 20–37 years) completed this double-blind, randomised study with two cycles of a 2-week run-in phase (10 g maltodextrin) followed by 5 weeks of 10 g FOS or BLEND once daily, separated by a 4-week wash-out interval. Abdominal symptoms and general wellbeing were documented by telephone interview or Internet twice weekly. Rectal sensations were assessed by a visual analogue scale during a rectal barostat test after FOS and BLEND treatment. Both FOS and BLEND induced more side effects than maltodextrin. Belching was more pronounced under FOS compared with BLEND (P = 0·09 for females; P = 0·01 for males), and for self-reported general wellbeing strong sex differences were reported (P = 0·002). Urgency scores during rectal barostat were higher with FOS than BLEND (P = 0·01). Faced with a growing range of supplemented food products, consumers may benefit from prebiotic mixtures which cause fewer abdominal side effects. Sex differences must be taken in consideration when food supplements are used.

The objective of the present study was to examine the effects of dietary Zn deficiency on the ex vivo cytokine production (IL-2, interferon-γ (IFN-γ), IL-6 and IL-10) of isolated thymocytes and splenocytes after mitogenic stimulation with concavalin A and to explore the role of corticosterone in this regulation. Weanling rats were assigned to one of four dietary treatments for 3 weeks: Zn-deficient ( < 1 mg Zn/kg diet, ad libitum), pair-fed (30 mg Zn/kg diet, limited to amount of feed as consumed by the Zn-deficient group), marginally Zn-deficient (10 mg Zn/kg diet, ad libitum) and control (30 mg Zn/kg diet, ad libitum). Thymocytes and splenocytes were isolated for cytokine stimulation and determination of T-cell phenotypes. Serum corticosterone concentrations were determined by ELISA. The Zn-deficient and pair-fed groups had 14-fold higher serum corticosterone concentrations compared with the marginally Zn-deficient and control groups (P < 0·0001). The proportions of thymocyte subsets were not altered in the Zn-deficient, pair-fed or marginally Zn-deficient groups; however, thymocyte IL-2 and IL-6 production in these groups was 33–54 % lower compared with the control group (P < 0·05). The Zn-deficient group had an 18–28 % lower proportion of new T-cells (TCRαβ+CD90+), but no difference in the proportion of new T-cells that were cytotoxic or helper. The Zn-deficient group had a 49–62 % lower production of Th1 cytokines (IL-2), but no difference in the production of Th2 cytokines (IL-6, IL-10) by stimulated splenocytes compared with the pair-fed, marginally Zn-deficient and control groups (P < 0·01). These results indicate that Zn status is associated with altered cytokine production, while in vivo corticosterone concentrations are not associated with ex vivo cytokine production.