The present review explores the interactions between sweeteners and enteroendocrine cells, and consequences for glucose absorption and insulin release. A combination of in vitro,in situ, molecular biology and clinical studies has formed the basis of our knowledge about the taste receptor proteins in the glucose-sensing enteroendocrine cells and the secretion of incretins by these cells. Low-energy (intense) sweeteners have been used as tools to define the role of intestinal sweet-taste receptors in glucose absorption. Recent studies using animal and human cell lines and knockout mice have shown that low-energy sweeteners can stimulate intestinal enteroendocrine cells to release glucagon-like peptide-1 and glucose-dependent insulinotropic peptide. These studies have given rise to major speculations that the ingestion of food and beverages containing low-energy sweeteners may act via these intestinal mechanisms to increase obesity and the metabolic syndrome due to a loss of equilibrium between taste receptor activation, nutrient assimilation and appetite. However, data from numerous publications on the effects of low-energy sweeteners on appetite, insulin and glucose levels, food intake and body weight have shown that there is no consistent evidence that low-energy sweeteners increase appetite or subsequent food intake, cause insulin release or affect blood pressure in normal subjects. Thus, the data from extensive in vivo studies in human subjects show that low-energy sweeteners do not have any of the adverse effects predicted by in vitro,in situ or knockout studies in animals.

Protein metabolism is known to be affected by dietary proteins, but the fundamental mechanisms that underlie the changes in protein metabolism are unclear. The aim of the present study was to test the effects of feeding growing rats with balanced diets containing soya protein isolate, zein and casein as the sole protein source on the expression of genes related to protein metabolism responses in skeletal muscle. The results showed that feeding a zein protein diet to the growing rats induced changes in protein anabolic and catabolic metabolism in their gastrocnemius muscles when compared with those fed either the reference protein casein diet or the soya protein isolate diet. The zein protein diet increased not only the mRNA levels and phosphorylation of mammalian target of rapamycin (mTOR), but also the mRNA expression of muscle atrophy F-box (MAFbx)/atrogin-1 and muscle ring finger 1 (MuRF1), as well as the forkhead box-O (FoxO) transcription factors involved in the induction of the E3 ligases. The amino acid profile of proteins seems to control signalling pathways leading to changes in protein synthesis and proteolysis.

To date, there has been no study of protein molecular structures affected by bioethanol processing in relation to protein nutritive values of the new co-products of bioethanol production. The objective of the present study was to investigate the relationship between protein molecular structures (in terms of protein α-helix and β-sheet spectral intensity and their ratio and amide I to amide II spectral intensity and their ratio) and protein rumen degradation kinetics (rate and extent), estimated protein intestinal digestibility and total truly absorbed protein in small intestine (metabolisable protein) in different types of dried distillers grains with solubles (DDGS), such as wheat DDGS, maize DDGS and blend DDGS (wheat:maize = 70:30). The protein molecular structures of the different types of DDGS affected by processing were identified using diffuse reflectance IR Fourier transform spectroscopy. The results showed that the protein structure α-helix to β-sheet ratio in the DDGS had a strongly negative correlation with estimated intestinal digestibility of ruminally undegraded protein (%dRUP, R − 0·95, P = 0·04), tended to have a significant correlation with the protein PC subfraction (which was undegradable and contained proteins associated with lignin and tannins and heat-damaged proteins) (R 0·91, P = 0·09) and had no correlation (P>0·10) with rumen degradation kinetics (rate and extent), total intestinally absorbed protein supply and degraded protein balance. However, the protein amide I to amide II ratio in the DDGS had a strongly positive correlation with soluble crude protein (CP) (R 0·99, P < 0·01), protein PA subfraction (which was instantaneously solubilised at time zero) (R 0·99, P < 0·01), protein PB2 subfraction (which was intermediately degradable) (R − 0·95, P = 0·04) and total digestible CP (R 0·95, P = 0·04). The amide I to amide II ratio also had strongly negative correlations with ruminally undegraded protein (%RUP: R − 0·96, P = 0·03) and the degraded protein balance (OEB: R − 0·97, P = 0·02), but had no correlation (P>0·10) with the total intestinally absorbed protein supply. Multiple regression results show that the protein structure α-helix to β-sheet ratio was a better predictor of %dRUP with R2 0·92. The amide I to II ratio was a better predictor of the degraded protein balance with R2 0·93 in the DDGS. In conclusion, the changes in the protein molecular structure α-helix to β-sheet ratio and the amide I to amide II ratio during bioethanol processing (either due to fermentation processing or due to heat drying) were highly associated with estimated protein intestinal digestibility and degraded protein balance, but were not associated with total intestinally absorbed protein supply from the DDGS to dairy cattle. The present study indicates that a potential novel method could be developed based on the protein molecular structure parameters to improve the estimation of protein value after a validation in a large-scale in vivo study is done.

During exercise, ammonia levels are related to the appearance of both central and peripheral fatigue. Therefore, controlling the increase in ammonia levels is an important strategy in ameliorating the metabolic response to exercise and in improving athletic performance. Free amino acids can be used as substrates for ATP synthesis that produces ammonia as a side product. Keto analogues act in an opposite way, being used to synthesise amino acids whilst decreasing free ammonia in the blood. Adult male rats were divided into four groups based on receiving either keto analogues associated with amino acids (KAAA) or a placebo and resistance exercise or no exercise. There was an approximately 40 % increase in ammonaemia due to KAAA supplementation in resting animals. Exercise increased ammonia levels twofold with respect to the control, with a smaller increase (about 20 %) in ammonia levels due to exercise. Exercise itself causes a significant increase in blood urea levels (17 %). However, KAAA reduced blood urea levels to 75 % of the pre-exercise values. Blood urate levels increased 28 % in the KAAA group, independent of exercise. Supplementation increased glucose levels by 10 % compared with control animals. Exercise did not change glucose levels in either the control or supplemented groups. Exercise promoted a 57 % increase in lactate levels in the control group. Supplementation promoted a twofold exercise-induced increase in blood lactate levels. The present results suggest that an acute supplementation of KAAA can decrease hyperammonaemia induced by exercise.

The effectiveness of conjugated linoleic acid (CLA) as a weight-loss nutraceutical continues to be debatable, suggesting that there may be value in exploring the physiological effects of the lesser-known isomers. The effects of the minor isomer, trans-8, cis-10 (t8, c10)-CLA, in the form of an equimolar mixture with the cis-9, trans-11 (c9, t11) isomer, on body weight and body composition, circulating glucose and lipid concentrations, and liver weights were studied in sixty male Syrian golden hamsters. Animals were randomised to receive for 28 d a semi-purified, hypercholesterolaemic diet (5 % dietary fat and 0·25 % cholesterol) supplemented at the 2 % level with either the t8, c10+c9, t11-CLA mixture, c9, t11-CLA or trans-10, cis-12 (t10, c12)-CLA replacing lard and safflower-seed oil (control). Results show that compared with control, the t8, c10+c9, t11-CLA mixture and t10, c12-CLA-fed animals had lower (P < 0·0001) fat mass following supplementation. Animals consuming t10, c12-CLA also possessed higher lean mass compared with control and c9, t11-CLA groups (P < 0·001). However, the livers of these animals were larger (P < 0·0001) compared with those in the control and other CLA groups. Body weights of the hamsters did not differ across the experimental groups. CLA treatments had no effect on serum glucose or lipid profile, except for inducing higher (P < 0·05) non-HDL-cholesterol concentration with t10, c12-CLA compared with the c9, t11 isomer. Overall, these results indicate that in male hamsters fed a hypercholesterolaemic diet, the t8, c10+c9, t11-CLA mixture does not have an impact on blood lipid profile, but is able to effectively reduce fat mass, without incurring an accompanying liver enlargement.

Different diets have distinct impacts on glucose homoeostasis, for which insulin sensitivity (IS) after a meal (postprandial IS) is highly relevant. Postprandial IS depends upon hepatic parasympathetic activation and glutathione content elevation. We tested the hypothesis that postprandial IS is compromised in high-fat diet (HFD)-induced obesity. Sprague–Dawley rats were fed a standard diet (STD, n 10), 1-week HFD (n 9) or 4-week HFD (n 8). IS was tested in postprandial state using the rapid IS test (RIST) before and after the blockade of the parasympathetic nerves (atropine, 1 mg/kg); parasympathetic-dependent IS was obtained from the difference between control and post-atropine RIST. Fasting IS was also assessed in the STD-fed rats (n 4) and 4-week HFD-fed rats (n 3) using the RIST. Whole-body fat and regional fat pads were heavier in the 1-week HFD-fed rats (79·8 (se 7·9) and 23·7 (se 1·0) g, respectively) or 4-week HFD-fed rats (106·5 (se 6·1) and 30·1 (se 1·4) g, respectively) than in the STD-fed rats (32·5 (se 3·7) and 13·7 (se 1·0) g, respectively; P < 0·001). Fasted-state IS was similar between the groups studied. Postprandial IS was higher in the STD-fed rats (185·8 (se 5·6) mg glucose/kg body weight (bw)) than in both the 1-week HFD-fed rats (108·8 (se 2·9) mg glucose/kg bw; P < 0·001) and 4-week HFD-fed rats (69·3 (se 2·6) mg glucose/kg bw; P < 0·001). Parasympathetic-dependent IS was impaired in both HFD-fed groups (STD, 108·9 (se 3·9) mg glucose/kg bw; 1-week HFD, 38·6 (se 4·2) mg glucose/kg bw; 4-week HFD, 5·4 (se 1·7) mg glucose/kg bw; P < 0·001). Total (postprandial) and parasympathetic-dependent IS correlated negatively with whole-body fat (R2 0·81 and 0·87) and regional adiposity (R2 0·85 and 0·79). In conclusion, fat accumulation induced by HFD is associated with postprandial insulin resistance, but not with fasting insulin resistance. HFD-associated postprandial insulin resistance is largely mediated by impairment of parasympathetic-dependent insulin action, which correlates with adiposity.

The aim of the present study was to investigate the cataract preventive effect of dietary histidine regimes in adult Atlantic salmon (Salmo salar L.) in seawater, both through manipulating the dietary histidine level and feeding period. Mean body weight of individually tagged Atlantic salmon at the start of the experiment was 1662 (sd 333) g. Low prevalence of mild cataracts were recorded in the beginning of June. Three fishmeal and fish oil-based extruded diets (crude protein: 375 g/kg and fat: 342 g/kg), differing only in histidine content (low (L): 9·3, medium (M): 12·8 and high (H): 17·2 g histidine/kg diets), were fed to duplicate net pens in seawater. The experimental period was divided into three seasons (June–July; July–September; September–October), each starting and ending with individual cataract examination, assessment of somatic data, and sampling of lens and muscle tissues for analysis of histidine and histidine derivatives. In July and September, a part of the population fed L- and H-histidine feeds were transferred (crossed over) to respective series of replicate net pens fed L-, M- and H-histidine diets (i.e. eleven experimental feeding groups at trial conclusion). The fish doubled their body weight from June to October, with no systematic effects on weight gain of dietary histidine feeding regimes. Development of severe cataracts was observed between July and September. The cataract severity was directly related to the dietary histidine level fed during the first and second periods. Feeding histidine-supplemented diets (M or H) in the first period from June to July mitigated later cataract outbreaks. The status of selected free imidazoles in muscle and lens tissues reflected the dietary histidine feeding regimes, relative to both feed concentration and feeding duration. The study shows the risk for cataract development for adult Atlantic salmon, 1 year after the transfer of salmon smolts from freshwater to seawater, which to a major extent can be prevented by histidine supplementation just before and during the early phase of cataract development.

There is concern regarding the possible negative effects of ingestion of dietary fibre on growth and intestinal Fe absorption in infants. The aim of the present study was to compare the effect of a fibre mixture on the growth and the intestinal absorption of Fe in rats with Fe-deficiency anaemia with that of a diet without fibres. Faecal weight and caecal pH were also evaluated. According to the Hb depletion–repletion model, twenty-two male weaned Wistar rats were fed the AIN93-G diet without Fe until Fe-deficiency anaemia was induced with Hb < 70 g/l. The anaemic rats were divided into two groups: (1) fibre mixture group – fed 100 g of fibre mixture/kg of diet (soya polysaccharide, inulin, resistant starch, Arabic gum, fructo-oligossaccharide and cellulose) (n 11); (2) control group – fed without fibres (n 11). All diets had 157 mg of ferric citrate (30 mg of elemental Fe) added to lead to recovery from anaemia. Fe intestinal absorption was measured by Hb repletion efficiency (HRE) and apparent Fe intestinal absorption. The HRE was 44·8 (sd 9·5) % in the fibre mixture group and 43·0 (sd 9·5) % in the control group (P = 0·664). The apparent Fe absorption was 46·2 (sd 16·5) and 47·2 (sd 10·2) % (P = 0·861) in the fibre mixture and control groups, respectively. The faecal weight median was 6·17 g in the fibre mixture group and 2·11 g in the control group (P < 0·001). The caecal pH was in the same order: 6·11 (sd 0·59) and 7·07 (sd 0·34) (P < 0·001). Both the groups consumed similar quantities of diet, and growth was similar in both the groups. The fibre mixture had no influence either on growth or on Fe intestinal absorption in rats recovering from anaemia. This mixture favoured an increase in faecal weight and a decrease in caecal pH.

The periparturient relaxation of immunity (PPRI) to parasites in mammals is sensitive to both metabolisable protein (MP) supply and animal genotype (different reproductive outputs). We tested the hypothesis that the sensitivity of PPRI to MP scarcity would not differ between different levels of reproductive output when nutrient intake is adjusted for associated differences in MP demand; this hypothesis assumes that PPRI has a nutritional basis only. Scottish Blackface (BF) and the more productive Mule (MU) ewes were infected with the abomasal parasite Teladorsagia circumcincta, and from day− 21 to day32 (day0 is parturition), they were fed restrictedly at either 0·8 (low protein (LP)) or 1·3 (high protein (HP)) times their breed-specific estimated MP requirement (n 18 for each breed–feeding treatment combination). During late pregnancy, LP feeding reduced ewe body weight gain in both breeds, tended to increase faecal egg count (FEC), but it did not affect plasma pepsinogen. During lactation, LP feeding reduced litter growth rate and ewe plasma urea and plasma albumin concentrations compared with HP feeding in both breeds. However, breed and feeding treatment interacted for ewe FEC, worm egg excretion and plasma pepsinogen, which were higher for the LP-MU ewes compared with the HP-MU and BF ewes. The lower degree of PPRI of the BF ewes during lactation compared with the MU ewes at a similar degree of MP scarcity suggests that the effect of reproductive output on nutritional sensitivity of PPRI cannot be explained by associated differences in nutrient demand only.

Vitamin D deficiency has been associated with increased risk of tuberculosis (TB). Changes from a traditional to a Westernised diet among Greenlanders have resulted in reduced serum vitamin D, leading to considerations of whether preventive vitamin D supplementation should be introduced. The association between vitamin D status and TB was examined to assess the feasibility of vitamin D supplementation in Greenland. This was examined in a case–control study involving seventy-two matched pairs of TB patients (cases) and controls aged 8–74 years. Cases were diagnosed with TB during 2004–6 based on clinical findings in combination with either (1) positive Mycobacterium tuberculosis culture, (2) characteristic X-ray abnormalities together with a positive tuberculin skin test or a positive interferon-γ release assay or (3) characteristic histology. Controls were individually matched on age ( ± 5 years), sex and district. Serum 25-hydroxyvitamin D (25(OH)D) concentrations were measured and OR of TB were the outcome. Compared with individuals with 25(OH)D concentrations between 75 and 140 nmol/l, individuals with concentrations < 75 nmol/l (OR 6·5; 95 % CI 1·8, 23·5) or>140 nmol/l (OR 6·5; 95 % CI 1·9, 22·2) had higher risks of active TB (P = 0·003; adjustment for alcohol and ethnicity). Supplementing individuals with low vitamin D to normalise serum 25(OH)D concentrations was estimated to result in a 29 % reduction in the number of TB cases. The study indicated that vitamin D supplementation may be beneficial to individuals with insufficient vitamin D concentrations but may increase the risk of TB among individuals with normal or high concentrations.

Changes in plasma endogenous and dietary antioxidants and oxidative stress markers were studied following two 90 min elite female soccer games separated by 72 h of either active or passive recovery. The active recovery group (n 8) trained for 1 h at 22 and 46 h after the first game (low-intensity cycling and resistance training), while the passive group rested (n 8). Blood samples were taken before the games; immediately after the games; 21, 45 and 69 h after the first game; and immediately after the second game. The oxidative stress markers and antioxidants were not affected by active recovery. The oxidative stress marker GSSG increased by the same extent after both the games, while the lipid peroxidation marker diacron-reactive oxygen metabolite remained unchanged. The endogenous antioxidants total glutathione and uric acid and ferric reducing/antioxidant power increased immediately after both the games with the same amplitude, while increases in cysteine, cysteine–glycine and total thiols reached significant levels only after the second game. The changes in dietary antioxidants after the first game were either rapid and persistent (tocopherols and ascorbic acid (AA) increased; polyphenols decreased) or delayed (carotenoids). This resulted in high pre-second game levels of tocopherols, AA and carotenoids. Polyphenols returned to baseline at 69 h, and were not affected by the second game. In conclusion, the soccer-associated dietary antioxidant defence, but not the endogenous antioxidant defence, is persistent. Similar acute oxidative stress and endogenous antioxidant responses and dissimilar dietary antioxidant reactions occur during two repeated female soccer games. Finally, the complex antioxidant response to soccer is not affected by active recovery training.

There is limited knowledge about the possible effect of unabsorbed dietary antioxidants that reach the large intestine on bowel habits. The aim of the present study was to investigate whether a dietary recommendation directed to increase diet total antioxidant capacity (TAC) is able to affect gut function in human subjects. In this cross-over intervention, nineteen subjects followed a high-TAC (HT) and a low-TAC (LT) diet for 2 weeks, which were comparable for energy, macronutrient, total dietary fibre and alcohol contents. At the end of each intervention period, the 48 h stool output was recorded. In the faecal samples obtained from a subset of nine subjects, moisture, pH, ammonia content, Lactobacillus and Bifidobacterium counts, faecal water antioxidants and genotoxicity were measured. A 3 d weighed food record was used to assess the diet composition during HT and LT diet intake. Significant increases in the intake of TAC, vitamins E and C and phenolic compounds were observed during the HT diet intake. The higher intake of antioxidants led to increased 48 h stool output (324 (sd 38) g in HT v. 218 (sd 22) g in LT), and to higher TAC and total phenolic concentrations in faecal water. No significant variation in the other measured parameters was observed between the diets. In conclusion, a diet selected to raise the intake of dietary antioxidants is able to increase stool bulk and antioxidant content of faeces.

Bioelectrical impedance vector analysis (BIVA) is a new method that is used for the routine monitoring of the variation in body fluids and nutritional status with assumptions regarding body composition values. The aim of the present study was to determine bivariate tolerance intervals of the whole-body impedance vector and to describe phase angle (PA) values for healthy term newborns aged 7–28 d. This descriptive cross-sectional study was conducted on healthy term neonates born at a low-risk public maternity. General and anthropometric neonatal data and bioelectrical impedance data (800 μA–50 kHz) were obtained. Bivariate vector analysis was conducted with the resistance–reactance (RXc) graph method. The BIVA software was used to construct the graphs. The study was conducted on 109 neonates (52·3 % females) who were born at term, adequate for gestational age, exclusively breast-fed and aged 13 (sd 3·6) d. We constructed one standard, reference, RXc-score graph and RXc-tolerance ellipses (50, 75 and 95 %) that can be used with any analyser. Mean PA was 3·14 (sd 0·43)° (3·12 (sd 0·39)° for males and 3·17 (sd 0·48)° for females). Considering the overlapping of ellipses of males and females with the general distribution, a graph for newborns aged 7–28 d with the same reference tolerance ellipse was defined for boys and girls. The results differ from those reported in the literature probably, in part, due to the ethnic differences in body composition. BIVA and PA permit an assessment without the need to know body weight and the prediction error of conventional impedance formulas.

The objective of the present study was to evaluate the effect of a paediatric tube feed supplemented with a multifibre mixture on the gut microbiota and nutritional and micronutrient status of children on long-term enteral nutrition (EN). A randomised, controlled, double-blind, cross-over trial (2 × 3 months) with a washout period of 1 month was carried out. Twenty-seven children (80 % neurologically impaired) aged 11·9 (sd 3·9) years, on long-term EN (4·8 (sd 3·9) years) were recruited. The analyses of the children's faecal pH, microbiota along with anthropometric measures, bowel movements and markers of blood micronutrient status were made. Twenty children completed the study. A significant increase in the proportion of stool bifidobacteria (+16·6 %, P < 0·05) was observed during the multifibre period than during the fibre-free period, together with a significant reduction in stool pH (P < 0·001). Stool frequency and consistency as well as growth did not differ between the two periods. There was a significant increase (P < 0·05) in plasma ferritin at the end of the fibre-free period, but plasma ferritin levels remained within normal ranges during both periods. No diet effects on other blood parameters were observed. In conclusion, addition of a multifibre mixture with prebiotic components to paediatric EN is well tolerated, promotes bifidobacteria and reduces stool pH, indicating an improved gut health.

Although increased concentrations of plasma inflammatory markers are not one of the criteria to diagnose the metabolic syndrome, low-grade systemic inflammation is receiving large attention as a metabolic syndrome component and cardiovascular risk factor. As several epidemiological studies have suggested a negative relationship between low-fat dairy consumption and the metabolic syndrome, we decided to investigate the effects of low-fat dairy consumption on inflammatory markers and adhesion molecules in overweight and obese subjects in an intervention study. Thirty-five healthy subjects (BMI>27 kg/m2) consumed, in a random order, low-fat dairy products (500 ml low-fat milk and 150 g low-fat yogurt) or carbohydrate-rich control products (600 ml fruit juice and three fruit biscuits) daily for 8 weeks. Plasma concentrations of TNF-α were decreased by 0·16 (sd 0·50) pg/ml (P = 0·070), and soluble TNF-α receptor-1 (s-TNFR-1) was increased by 110·0 (sd 338·4) pg/ml (P = 0·062) after the low-fat dairy period than after the control period. s-TNFR-2 was increased by 227·0 (sd 449·0) pg/ml (P = 0·020) by the dairy intervention. As a result, the TNF-α index, defined as the TNF-α:s-TNFR-2 ratio, was decreased by 0·000053 (sd 0·00 012) (P = 0·015) after the dairy diet consumption. Low-fat dairy consumption had no effect on IL-6, monocyte chemoattractant protein-1, intracellular adhesion molecule-1 and vascular cell adhesion molecule-1 concentrations. The present results indicate that in overweight and obese subjects, low-fat dairy consumption for 8 weeks may increase concentrations of s-TNFR compared with carbohydrate-rich product consumption, but that it has no effects on other markers of chronic inflammation and endothelial function.

Increased intake of marine long-chain n-3 PUFA (n-3 LCPUFA) may decrease the risk of CVD and reduce mortality by lowering serum TAG and blood pressure (BP). Furthermore, n-3 LCPUFA may affect novel CVD risk markers related to inflammation and vascular function. The objective of the present study was to examine the effect of farmed trout on novel and traditional CVD risk markers in healthy men, and to evaluate whether this was affected by the aquacultural feed regime. We performed a parallel, 8-week intervention study in which sixty-eight healthy male volunteers were randomised to consume either a daily meal with 150 g farmed trout raised on either marine or vegetable-based feed, or a reference meal containing 150 g chicken. Twenty-four hour BP, pulse wave velocity, augmentation index, fatty acid composition of erythrocyte (RBC), and concentrations of TAG, HDL-cholesterol, LDL-cholesterol, glucose, insulin, C-reactive protein (CRP) and other markers of inflammation were measured at weeks 0 and 8. RBC content of total n-3 LCPUFA, both EPA and DHA, was significantly higher among men consuming trout raised on marine feed compared with men consuming the vegetable-fed trout or chicken. The three intervention groups did not differ significantly with respect to any of the other outcome variables, although there were trends towards associations between the changes in RBC n-3 LCPUFA and those in BP and CRP. In the present study, we conclude that we could not confirm the fish oil-induced reduction in CVD risk markers after daily consumption of trout with high or low n-3 LCPUFA content. However, trout raised on vegetable-based feed had less pronounced impact on RBC n-3 LCPUFA status.

Whole cereal grain foods are rich in phytate, a Ca chelator, and could increase the risk of hip fracture. The objective of the present study was to investigate the association between baseline whole grain intake and incident hip fracture. In the present study, 29 192 women who at baseline in 1986 were aged 55–69 years, free of diabetes, and reported a plausible energy intake of 2508–20 900 kJ/d and reported no fracture since the age of 35 years were followed. Hip fracture (n 746) was self-reported in five questionnaires through 2004. Of 1451 hip fractures identified passively by Medicare linkage through 31 December 2004 (Medicare hip fracture), 507 had also been self-reported. Whole grain intake was inversely related to Medicare hip fracture (Ptrend = 0·02), but it was unrelated to self-reported hip fracture (Ptrend = 0·27). The hazard ratio in the highest to lowest quintile of whole grain intake for incident Medicare-only hip fracture (n 944) was 0·66 (95 % CI 0·53, 0·82) after adjustment for age, energy intake, education, BMI, waist-to-hip ratio, farm residence, physical activity, oestrogen use, smoking, alcohol use, history of cancer and other dietary variables. Medicare-only cases may have failed to self-report due to severe illness; hazard ratio for total mortality after hip fracture was 2·92 (2·37, 3·59) for Medicare-only cases v. Medicare-confirmed self-reported cases. In conclusion, in this cohort, the inverse association between whole grain intake and hip fracture was explained by ascertainment bias. Whole grain intake may increase the ability to respond to a questionnaire and self-report hip fracture, and could reflect less undocumented frailty.

The WHO (2001) recommends exclusive breast-feeding and delaying the introduction of solid foods to an infant's diet until 6 months postpartum. However, in many countries, this recommendation is followed by few mothers, and earlier weaning onto solids is a commonly reported global practice. Therefore, this prospective, observational study aimed to assess compliance with the WHO recommendation and examine weaning practices, including the timing of weaning of infants, and to investigate the factors that predict weaning at ≤ 12 weeks. From an initial sample of 539 pregnant women recruited from the Coombe Women and Infants University Hospital, Dublin, 401 eligible mothers were followed up at 6 weeks and 6 months postpartum. Quantitative data were obtained on mothers’ weaning practices using semi-structured questionnaires and a short dietary history of the infant's usual diet at 6 months. Only one mother (0·2 %) complied with the WHO recommendation to exclusively breastfeed up to 6 months. Ninety-one (22·6 %) infants were prematurely weaned onto solids at ≤ 12 weeks with predictive factors after adjustment, including mothers’ antenatal reporting that infants should be weaned onto solids at ≤ 12 weeks, formula feeding at 12 weeks and mothers’ reporting of the maternal grandmother as the principal source of advice on infant feeding. Mothers who weaned their infants at ≤ 12 weeks were more likely to engage in other sub-optimal weaning practices, including the addition of non-recommended condiments to their infants’ foods. Provision of professional advice and exploring antenatal maternal misperceptions are potential areas for targeted interventions to improve compliance with the recommended weaning practices.

The aim of this analysis was to investigate the strength of the association between sugar intake and treatment for dental decay in children in Scotland, and the impact of tooth brushing frequency on this association. The Survey of Sugar Intake among Children in Scotland was carried out in 2006 in those aged 3–17 years. Diet was assessed using the Scottish Collaborative Group FFQ, and interviews were carried out by trained fieldworkers who asked about dental health. A total of 1700 interviews were carried out, and 1512 FFQ were returned. Of the children, 56 % had received treatment for decay (fillings or teeth removed due to decay). Intake of non-milk extrinsic sugars (NMES), but not total sugar, increased the risk of having had treatment for decay: adjusted OR 1·84 (95 % CI 1·28, 2·64) for the highest ( ≥ 20·0 % food energy) v. lowest ( ≤ 14·8 % food energy) tertile of NMES intake. This raised risk remained in children who reported brushing their teeth at least twice a day. Compared with children who reported brushing their teeth at least twice a day and were in the lowest tertile of NMES intake, children who reported brushing their teeth once a day or less and were in the highest tertile of NMES intake were over three times more likely to have received treatment for decay (adjusted OR 3·39, 95 % CI 1·97, 5·82). In order to improve dental health in children in Scotland, dental health strategies must continue to stress the importance of both reduced NMES intake and good oral hygiene.

We evaluated the accuracy of skinfold thicknesses, BMI and waist circumference for the prediction of percentage body fat (PBF) in a representative sample of 372 Swiss children aged 6–13 years. PBF was measured using dual-energy X-ray absorptiometry. On the basis of a preliminary bootstrap selection of predictors, seven regression models were evaluated. All models included sex, age and pubertal stage plus one of the following predictors: (1) log-transformed triceps skinfold (logTSF); (2) logTSF and waist circumference; (3) log-transformed sum of triceps and subscapular skinfolds (logSF2); (4) log-transformed sum of triceps, biceps, subscapular and supra-iliac skinfolds (logSF4); (5) BMI; (6) waist circumference; (7) BMI and waist circumference. The adjusted determination coefficient () and the root mean squared error (RMSE; kg) were calculated for each model. LogSF4 ( 0·85; RMSE 2·35) and logSF2 ( 0·82; RMSE 2·54) were similarly accurate at predicting PBF and superior to logTSF ( 0·75; RMSE 3·02), logTSF combined with waist circumference ( 0·78; RMSE 2·85), BMI ( 0·62; RMSE 3·73), waist circumference ( 0·58; RMSE 3·89), and BMI combined with waist circumference ( 0·63; RMSE 3·66) (P < 0·001 for all values of ). The finding that logSF4 was only modestly superior to logSF2 and that logTSF was better than BMI and waist circumference at predicting PBF has important implications for paediatric epidemiological studies aimed at disentangling the effect of body fat on health outcomes.