Iodine is required for adequate thyroid hormone production, which is essential for brain development, particularly in the first trimester of pregnancy. Milk is the principal source of iodine in UK diets, and while small studies in Europe have shown organic milk to have a lower iodine concentration than conventional milk, no such study has been conducted in Britain. In view of the increasing popularity of organic milk in the UK, we aimed to compare the iodine concentration of retail organic and conventional milk and to evaluate regional influences in iodine levels. Samples of organic milk (n 92) and conventional milk (n 80), purchased from retail outlets in sixteen areas of the UK (southern England, Wales and Northern Ireland), were analysed for iodine using inductively coupled plasma MS. The region of origin of the milk was determined from information on the label. Organic milk was 42·1 % lower in iodine content than conventional milk (median iodine concentration 144·5 v. 249·5 ng/g; P < 0·001). There was no difference in the iodine concentration of either conventional or organic milk by area of purchase. However, a difference was seen in iodine concentration of organic milk by region of origin (P < 0·001). The lower iodine concentration of organic milk has public-health implications, particularly in view of emerging evidence of iodine deficiency in UK population sub-groups, including pregnant women. Individuals who choose organic milk should be aware that their iodine intake may be compromised and should ensure adequate iodine intake from alternative sources.

Formation of advanced glycation end products (AGE) plays a key role in the several pathophysiologies associated with ageing and diabetes, such as arthritis, atherosclerosis, chronic renal insufficiency, Alzheimer's disease, nephropathy, neuropathy and cataract. This raises the possibility of inhibition of AGE formation as one of the approaches to prevent or arrest the progression of diabetic complications. Previously, we have reported that some common dietary sources such as fruits, vegetables, herbs and spices have the potential to inhibit AGE formation. Flavonoids are abundantly found in fruits, vegetables, herbs and spices, and rutin is one of the commonly found dietary flavonols. In the present study, we have demonstrated the antiglycating potential and mechanism of action of rutin using goat eye lens proteins as model proteins. Under in vitro conditions, rutin inhibited glycation as assessed by SDS-PAGE, AGE-fluorescence, boronate affinity chromatography and immunodetection of specific AGE. Further, we provided insight into the mechanism of inhibition of protein glycation that rutin not only scavenges free-radicals directly but also chelates the metal ions by forming complexes with them and thereby partly inhibiting post-Amadori formation. These findings indicate the potential of rutin to prevent and/or inhibit protein glycation and the prospects for controlling AGE-mediated diabetic pathological conditions in vivo.

An increased intestinal permeability is associated with several diseases. Previously, we have shown that dietary Ca decreases colonic permeability in rats. This might be explained by a calcium-phosphate-induced increase in luminal buffering capacity, which protects against an acidic pH due to microbial fermentation. Therefore, we investigated whether dietary phosphate is a co-player in the effect of Ca on permeability. Rats were fed a humanised low-Ca diet, or a similar diet supplemented with Ca and containing either high, medium or low phosphate concentrations. Chromium-EDTA was added as an inert dietary intestinal permeability marker. After dietary adaptation, short-chain fructo-oligosaccharides (scFOS) were added to all diets to stimulate fermentation, acidify the colonic contents and induce an increase in permeability. Dietary Ca prevented the scFOS-induced increase in intestinal permeability in rats fed medium- and high-phosphate diets but not in those fed the low-phosphate diet. This was associated with higher faecal water cytotoxicity and higher caecal lactate levels in the latter group. Moreover, food intake and body weight during scFOS supplementation were adversely affected by the low-phosphate diet. Importantly, luminal buffering capacity was higher in rats fed the medium- and high-phosphate diets compared with those fed the low-phosphate diet. The protective effect of dietary Ca on intestinal permeability is impaired if dietary phosphate is low. This is associated with a calcium phosphate-induced increase in luminal buffering capacity. Dragging phosphate into the colon and thereby increasing the colonic phosphate concentration is at least part of the mechanism behind the protective effect of Ca on intestinal permeability.

Recent observations indicate that human milk oligosaccharides (HMO) are involved in a variety of physiological processes in infants. Their metabolic fate, however, is virtually unknown. We investigated metabolic aspects in infants after endogenous 13C-labelling of HMO. An oral bolus of natural and 13C-labelled galactose (Gal; 23 g Gal+4 g 13C-Gal) was given to ten lactating women. Aliquots of milk at each nursing as well as breath samples from the mothers and urine from their infants were collected over 36 h. The 13C-enrichment of HMO and their renal excretion was determined by isotope ratio-MS; characterisation was achieved by fast atom bombardment-MS. After the Gal bolus was given, an immediate 13C-enrichment in milk and in infants' urine was observed which lasted 36 h. Mass spectrometric analysis of 13C-enriched urinary fractions confirmed the excretion of a variety of neutral and acidic HMO without metabolic modification of their structures. Components with glucose split off at the reducing end were also detectable. Quantitative data regarding the infants' intake of lacto-N-tetraose and its monofucosylated derivative lacto-N-fucopentaose II ranged from 50 to 160 mg with each suckling, respectively; renal excretion of both components varied between 1 and 3 mg/d. Since the intake of individual HMO by the infants was in the range of several hundred mg per suckling, i.e. several g/d, and some of these components were excreted in mg amounts as intact HMO with the infants' urine, not only local but also systemic effects might be expected.

In addition to being a risk factor for adverse outcomes of pregnancy, maternal obesity may play a role in determining the long-term disease patterns observed in the resulting offspring, with metabolic and dietary factors directly programming fetal development. The present study evaluated the potential for feeding rats an obesogenic cafeteria diet (O) pre-pregnancy, during pregnancy, during lactation and for the offspring post-weaning, to programme glucose tolerance. Early-life exposure to an O diet had no significant effect on offspring food intake. Early-life programming associated with O feeding to induce maternal obesity was associated with reduced adiposity in offspring weaned onto low-fat chow. Adult offspring exposed to an O diet in early life and weaned on a chow diet had low fasting glucose and insulin concentrations and appeared to be more sensitive to insulin during an intraperitoneal glucose tolerance test. When weaned on an O diet, male offspring were more prone to glucose intolerance than females. On the basis of the area under the glucose curve, maternal O feeding at any point from pre-mating to lactation was associated with impaired glucose tolerance. The mechanism for this was not identified, although increased hepatic expression of Akt2 may have indicated disturbance of insulin signalling pathways. The observations in the present study confirm that maternal overnutrition and obesity during pregnancy are risk factors for metabolic disturbance in the resulting offspring. Although the effects on glucose homeostasis were independent of offspring adiposity, the programming of a glucose-intolerant phenotype was only observed when offspring were weaned on a diet that induced greater fat deposition.

It is known that Ca therapy may have anti-obesity effects. Since early weaning leads to obesity, hyperleptinaemia and insulin resistance, we studied the effect of dietary Ca supplementation in a rat model. Lactating rats were separated into two groups: early weaning (EW) – dams were wrapped with a bandage to interrupt lactation in the last 3 d of lactation and control (C) – dams whose pups had free access to milk during the entire lactation period (21 d). At 120 d, EW and C offspring were subdivided into four groups: (1) C, received standard diet; (2) CCa, received Ca supplementation (10 g of calcium carbonate/kg of rat chow); (3) EW, received standard diet; (4) EWCa, received Ca supplementation similar to CCa. The rats were killed at 180 d. The significance level was at P < 0·05. Adult EW offspring displayed hyperphagia (28 %), higher body weight (9 %) and adiposity (77 %), hyperleptinaemia (twofold increase), hypertriacylglycerolaemia (64 %), hyperglycaemia (16 %), higher insulin resistance index (38 %) and higher serum 25-hydroxyvitamin D3 (fourfold increase), but lower adiponectinaemia:adipose tissue ratio (44 %). In addition, they showed Janus tyrosine kinase 2 and phosphorylated signal transducer and activator of transcription 3 underexpression in hypothalamus (36 and 34 %, respectively), suggesting leptin resistance. Supplementation of Ca for 2 months normalised these disorders. The EW group had no change in serum insulin, thyroxine or triiodothyronine, and Ca treatment did not alter these hormones. In conclusion, we reinforced that early weaning leads to late development of some components of the metabolic syndrome and leptin resistance. Dietary Ca supplementation seems to protect against the development of endocrine and metabolic disorders in EW offspring, maybe through vitamin D inhibition.

We aimed to determine the effects of variations in dietary composition on equine gut microbiota and their fermentation products, and proposed that dietary modifications profoundly affect microbial ecosystems and their metabolites. Bacterial communities within the large intestine of three groups of horses were compared using oligonucleotide-RNA hybridisation methodology. Each group consisting of six horses was maintained on (1) a grass-only diet, (2) a concentrate diet (i.e. supplemented with hydrolysable carbohydrates) and (3) a concentrate diet but horses were affected by simple colonic obstruction and distension (SCOD), a prevalent form of dietary-induced intestinal disease. We show that in response to dietary change and intestinal disease, there is a progressive and significant increase in Lachnospiraceae, the Bacteroidetes assemblage and the lactic acid-producing, Bacillus–Lactobacillus–Streptococcus (BLS) group. In contrast, there is a corresponding decrease in the proportion of obligate fibrolytic, acid-intolerant bacteria, Fibrobacter and Ruminococcaceae. Assessment of monocarboxylic acids indicated that there are significantly higher concentrations of lactic acid in the colonic contents of horses maintained on a concentrate diet and those suffering from SCOD, correlating with the observed increase in the population abundance of the BLS group. However, the population size of the Veillonellaceae (lactate utilisers) remained constant in each study group. The inability of this group to respond to increased lactic acid may be a contributory factor to the build-up of lactic acid observed in horses fed a concentrate diet and those suffering from SCOD.

The aim of the present study was to analyse the bacteriological factors during the process of dental alveolitis, relating it to a higher incidence of bacteraemia in adult rats subjected to neonatal malnutrition. We used forty male Wistar rats, suckled by mothers fed a diet during lactation containing 17 % protein in the nourished group (N) or 8 % protein in the undernourished group (UN). After weaning, the animals were given the Labina standard diet. After 90 d, these animals underwent upper right incisor extraction and induction of alveolitis. The oral microbiota was obtained using a swab and blood culture through venous blood. These procedures were performed before the extraction, 5 min after extraction, on the 21st day after alveolitis for groups N-21 and UN-21 and on the 28th day after alveolitis for groups N-28 and UN-28. Data were expressed as means and standard deviations for parametric data, and as medians and interquartile intervals for non-parametric data. Statistical significance was considered by assuming a critical level of 5 %. Before and after extraction, lower bacterial growth was observed per colony-forming unit (CFU) in the perialveolar region of the upper right incisors of undernourished animals, while the opposite was true after alveolitis, when a larger number of CFU was observed in these animals. The percentage of positive blood cultures obtained after alveolitis was greater in the undernourished animals. The present study thus demonstrated the influence of neonatal malnutrition in the perialveolar microbiota and in the development of bacteraemia after dental alveolitis.

The present investigation was carried out to evaluate the hepatoprotective effect of probiotic fermented milk (FM) containing Lactobacillus rhamnosus GG and Lactobacillus casei strain Shirota, alone as well as in combination with chlorophyllin (CHL) as an antioxidant agent in male Wistar rats administered aflatoxin-B1 (AFB1). AFB1 was injected intraperitoneally at the rate of 450 μg/kg body weight per animal twice a week for 6 weeks, maintaining an equal time interval between the two consecutive AFB1 administrations. A total of 125 male Wistar rats were randomly allocated to five groups, each group having twenty-five animals. Group I was offered FM containing L. rhamnosus GG and L. casei strain Shirota. Group II was administered AFB1 and served as the control group; group III was administered FM-AFB1, in which besides administering AFB1, FM was also offered. Group IV was offered CHL and AFB1, and group V was offered both FM and CHL along with AFB1. The rats were euthanised at the 15th and 25th week of the experiment and examined for the biochemical and hepatopathological profile. A significant reduction in thiobarbituric acid-reactive substances (TBARS) was observed in the FM–CHL–AFB1 group compared with the AFB1 control group. FM alone or in combination with CHL was found to show a significant (P < 0·05) hepatoprotective effect by lowering the levels of TBARS and by enhancing the activities of antioxidant enzymes such as glutathione peroxidase, superoxide dismutase, catalase and glutathione-S-transferase, indicating that probiotic FM alone or in combination with CHL possesses a potent protective effect against AFB1-induced hepatic damage.

Previous studies have suggested that Lingzhi (Ganoderma lucidum) has antioxidant effects and possibly beneficial effects on blood pressure, plasma lipids and glucose, but these have not been confirmed in subjects with mild hypertension or hyperlipidaemia. The objective of the present study was to assess the cardiovascular, metabolic, antioxidant and immunomodulatory responses to therapy with Lingzhi in patients with borderline elevations of blood pressure and/or cholesterol in a controlled cross-over trial. A total of twenty-six patients received 1·44 g Lingzhi daily or matching placebo for 12 weeks in a randomised, double-blind, cross-over study with placebo-controlled run-in and cross-over periods. Body weight, blood pressure, metabolic parameters, urine catecholamines and cortisol, antioxidant status and lymphocyte subsets were measured after each period. Lingzhi was well tolerated and data from twenty-three evaluable subjects showed no changes in BMI or blood pressure when treated with Lingzhi or placebo. Plasma insulin and homeostasis model assessment-insulin resistance were lower after treatment with Lingzhi than after placebo. TAG decreased and HDL-cholesterol increased with Lingzhi but not with placebo in the first treatment period, but significant carry-over effects prevented complete analysis of these parameters. Urine catecholamines and cortisol, plasma antioxidant status and blood lymphocyte subsets showed no significant differences across treatments. Results indicate that Lingzhi might have mild antidiabetic effects and potentially improve the dyslipidaemia of diabetes, as shown previously in some animal studies. Further studies are desirable in patients with hyperglycaemia.

A detailed understanding of the underlying drivers of obesity-risk behaviours is needed to inform prevention initiatives, particularly for individuals of low socioeconomic position who are at increased risk of unhealthy weight gain. However, few studies have concurrently considered factors in the home and local neighbourhood environments, and little research has examined determinants among children from low socioeconomic backgrounds. The present study examined home, social and neighbourhood correlates of BMI (kg/m2) in children living in disadvantaged neighbourhoods. Cross-sectional data were collected from 491 women with children aged 5–12 years living in forty urban and forty rural socioeconomically disadvantaged areas (suburbs) of Victoria, Australia in 2007 and 2008. Mothers completed questionnaires about the home environment (maternal efficacy, perceived importance/beliefs, rewards, rules and access to equipment), social norms and perceived neighbourhood environment in relation to physical activity, healthy eating and sedentary behaviour. Children's height and weight were measured at school or home. Linear regression analyses controlled for child sex and age. In multivariable analyses, children whose mothers had higher efficacy for them doing physical activity tended to have lower BMI z scores (B = − 0·04, 95 % CI − 0·06, − 0·02), and children who had a television (TV) in their bedroom (B = 0·24, 95 % CI 0·04, 0·44) and whose mothers made greater use of food as a reward for good behaviour (B = 0·05, 95 % CI 0·01, 0·09) tended to have higher BMI z scores. Increasing efficacy among mothers to promote physical activity, limiting use of food as a reward and not placing TV in children's bedrooms may be important targets for future obesity prevention initiatives in disadvantaged communities.

Several regulatory bodies have approved a health claim on the cholesterol-lowering effects of oat β-glucan at levels of 3·0 g/d. The present study aimed to test whether 1·5 g/d β-glucan provided as ready-to-eat oat flakes was as effective in lowering cholesterol as 3·0 g/d from oats porridge. A 6-week randomised controlled trial was conducted in eighty-seven mildly hypercholesterolaemic ( ≥ 5 mmol/l and < 7·5 mmol/l) men and women assigned to one of three diet arms (25 % energy (E%) protein; 45 E% carbohydrate; 30 E% fat, at energy requirements for weight maintenance): (1) minimal β-glucan (control); (2) low-dose oat β-glucan (1·5 g β-glucan; oats low – OL) or (3) higher dose oat β-glucan (3·0 g β-glucan; oats high – OH). Changes in total cholesterol and LDL-cholesterol (LDL-C) from baseline were assessed using a linear mixed model and repeated-measures ANOVA, adjusted for weight change. Total cholesterol reduced significantly in all groups ( − 7·8 (sd 13·8) %, − 7·2 (sd 12·4) % and − 5·5 (sd 9·3) % in the OH, OL and control groups), as did LDL-C ( − 8·4 (sd 18·5) %, − 8·5 (sd 18·5) % and − 5·5 (sd 12·4) % in the OH, OL and control groups), but between-group differences were not significant. In responders only (n 60), β-glucan groups had higher reductions in LDL-C ( − 18·3 (sd 11·1) % and − 18·1 (sd 9·2) % in the OH and OL groups) compared with controls ( − 11·7 (sd 7·9) %; P = 0·044). Intakes of oat β-glucan were as effective at doses of 1·5 g/d compared with 3 g/d when provided in different food formats that delivered similar amounts of soluble β-glucan.

Glycogen stored in skeletal muscle is the main fuel for endurance exercise. The present study examined the effects of oral hydroxycitrate (HCA) supplementation on post-meal glycogen synthesis in exercised human skeletal muscle. Eight healthy male volunteers (aged 22·0 (se 0·3) years) completed a 60-min cycling exercise at 70–75 % and received HCA or placebo in a crossover design repeated after a 7 d washout period. They consumed 500 mg HCA or placebo with a high-carbohydrate meal (2 g carbohydrate/kg body weight, 80 % carbohydrate, 8 % fat, 12 % protein) for a 3-h post-exercise recovery. Muscle biopsy samples were obtained from vastus lateralis immediately and 3 h after the exercise. We found that HCA supplementation significantly lowered post-meal insulin response with similar glucose level compared to placebo. The rate of glycogen synthesis with the HCA meal was approximately onefold higher than that with the placebo meal. In contrast, GLUT4 protein level after HCA supplementation was significantly decreased below the placebo level, whereas expression of fatty acid translocase (FAT)/CD36 mRNA was significantly increased above the placebo level. Furthermore, HCA supplementation significantly increased energy reliance on fat oxidation, estimated by the gaseous exchange method. However, no differences were found in circulating NEFA and glycerol levels with the HCA meal compared with the placebo meal. The present study reports the first evidence that HCA supplementation enhanced glycogen synthesis rate in exercised human skeletal muscle and improved post-meal insulin sensitivity.

n-3 Fatty acids are recognised as influencing both wound healing and immunity. We assessed the impact of a fish oil- and micronutrient-enriched formula (study formula) on the healing of pressure ulcers and on immune function in critically ill patients in an intensive care unit. A total of forty patients with pressure ulcers and receiving nutritional support were enrolled (intervention group, n 20, received study formula; and a control group, n 20, received an isoenergetic formula). Total and differential leucocyte count and percentage of adhesion molecule positive granulocyte and lymphocyte cells (CD11a, CD11b, CD18 and CD49b) were measured on days 0, 7 and 14. Percentage of positive lymphocytes for CD54, CD49b, CD49d and CD8 were also measured on days 0, 7 and 14. The state of pressure ulcers was assessed by using the pressure ulcer scale for healing tool score on days 7, 14 and 28 of treatment. No between-group differences in patient demographics, anthropometry or diagnostic class were observed. Patients who received the study formula showed significant increases in the percentage of positive CD18 and CD11a lymphocytes and of CD49b granulocytes as compared to controls (P < 0·05). While the severity of pressure ulcers was not significantly different between the two groups on admission, severity increased significantly over time for the control group (P < 0·05), but not for the study group. The present study suggests that a fish oil- and micronutrient-enriched formula may prevent worsening of pressure ulcers and that this effect may be mediated by an effect on adhesion molecule expression.

Increased plasma concentrations of small LDL particles denote an atherogenic lipoprotein phenotype (ALP) that is correlated with increased circulating TAG and reduced HDL-cholesterol. Principal component analyses of subfraction concentrations have previously been used in the Swedish population-based Malmö Diet and Cancer (MDC) cohort to identify three independent components, one pattern representing the ALP. The aim of the present study was to examine the associations between macronutrient intakes and the principal component representing the ALP. We examined 4301 healthy subjects (46–68 years old, 60 % women) at baseline in the MDC cohort. Dietary data were collected using a modified diet history method. Plasma lipoprotein subfractions were measured using a high-resolution ion mobility method. The principal component corresponding to the ALP was significantly associated with a higher intake of disaccharides, and inversely related to protein and alcohol consumption (P < 0·001 for all). The present findings indicate that the ALP may be improved by a low intake of disaccharides, and moderate intakes of protein and alcohol.

We studied the associations of a difference in linoleic acid or carbohydrate intake with plasma cholesterol levels and risk of CHD in a prospective cohort study in the Netherlands. Data on diet (FFQ) and plasma total and HDL-cholesterol were available at baseline (1993–7) of 20 069 men and women, aged 20–65 years, who were initially free of CVD. Incidence of CHD was assessed through linkage with mortality and morbidity registers. During an average of 10 years of follow-up, 280 CHD events occurred. The intake of linoleic acid ranged from 3·6 to 8·0 % of energy (en%), whereas carbohydrate intake ranged from 47·6 to 42·5 en% across quintiles of linoleic acid intake. Linoleic acid intake was inversely associated with total cholesterol and HDL-cholesterol in women but not in men. Linoleic acid intake was not associated with the ratio of total to HDL-cholesterol. No association was observed between linoleic acid intake and CHD incidence, with hazard ratios varying between 0·83 and 1·00 (all P>0·05) compared to the bottom quintile. We conclude that a 4–5 en% difference in linoleic acid or carbohydrate intake did not translate into either a different ratio of total to HDL-cholesterol or a different CHD incidence.

High concentrations of fluoride (F) in powdered milk (formula milk) can have adverse health effects on the body. The F concentration in powdered milk was analysed in Iran in 2010. A total of twelve commercial brands of highly consumed powdered milk were selected to analyse the F content through the standard F ion-selective electrode method. From each brand, three samples with different production dates were selected. The means and standard deviation for F concentration in all the samples was 1·73 (sd 0·3) μg F/g. The minimum and maximum F content in powdered milk brands Humana2 and Humana3 was 1·32 (sd 0·1) and 2·36 (sd 0·3) μg F/g, respectively. The study revealed that there was no significant difference in F concentration in the samples that belonged to various dates. Humana3 had a high F concentration (with an average of 2·36 (sd 0·3) μg F/g), which can be a risk factor for increased dental fluorosis, especially when being prepared using water with a high content of F.

Poor vitamin D status is common in older people and results in osteoporosis; osteomalacia is associated with a wide range of non-communicable diseases and has potential effects on poor health outcomes. Pain is also common in older people and can be substantially disabling. The aim of the present analysis is to investigate associations between serum 25-hydroxy vitamin D (25(OH)D) and self-reported current symptoms of pain in a cross-sectional, nationally representative sample of 2070 adults aged ≥ 65 years living in the community in England in 2005. Measurements included serum 25(OH)D, pain status and covariates, namely, age, sex, social class, season of examination, use of vitamin supplements and physical health status. Results show that the symptoms of moderate/extreme pain (present in 53 % of the sample) were associated with poor vitamin D status, independent of other covariates. Particular advantages of the present study were the presence of directly measured vitamin D levels and a large and nationally representative sample. Poor vitamin D status is common and an associated risk factor for pain in older people living in northern latitudes. The direction of causation cannot be inferred from a cross-sectional study and further prospective research is required to clarify this. Regardless of the direction of causation, the relationship is potentially of high public health importance because of the adverse impact of both states on well-being. It is important that older people in pain are screened for vitamin D status and provided with appropriate interventions.

Obesity and sarcopenia are health problems associated with ageing. The present study modelled the longitudinal changes in body composition of healthy men, aged from 20 to 96 years, and evaluated the fidelity of BMI to identify age-dependent changes in fat mass and fat-free mass. The data from 7265 men with multiple body composition determinations (total observations 38 328) were used to model the age-related changes in body mass, fat mass, fat-free mass, BMI and percentage of body fat. Changes in fat mass and fat-free mass were used to evaluate the fidelity of BMI and to detect body composition changes with ageing. Linear mixed regression models showed that all trajectories of body composition with healthy ageing were quadratic. Fat mass, BMI and percentage of body fat increased from age 20 years and levelled off at approximately 80 years. Fat-free mass increased slightly from age 20 to 47 years and then declined at a non-linear rate with ageing. Levels of aerobic exercise had a positive influence on fat mass and a slight negative effect on fat-free mass. BMI and percentage of body fat were sensitive in detecting the increase in fat mass that occurred with healthy ageing, but failed to identify the loss of fat-free mass that started at age 47 years.