The SNP rs1260326 (P446L) and rs1799884 ( − 30G>A) for the glucokinase regulatory protein (GCKR) and glucokinase (GCK) genes, respectively, have been associated with opposing effects on TAG and glucose concentrations. However, their genetic modulation by diet (dietary patterns or foods) remains to be investigated. We studied 945 high-cardiovascular risk subjects aged 67 (sd 6) years who participated in the PREvención con DIeta MEDiterránea-Valencia Study. Demographic, clinical, biochemical and genetic data were obtained. Adherence to the Mediterranean diet (MD) and food intake were measured by validated questionnaires. Carriers of the L allele of GKCR had significantly higher TAG concentrations (PP: 1·34 (sd 0·05) mmol/l v. PL+LL: 1·54 (sd 0·03) mmol/l; P= 0·014) and LL carriers had lower glucose concentrations (PL+PP: 6·85 (sd 0·08) mmol/l v. LL: 6·40 (sd 0·16) mmol/l; P= 0·032) after multivariate adjustment. Conversely, homozygous subjects for the variant allele (A) in the GCK gene had significantly lower TAG (GG+GA: 1·48 (sd 0·03) mmol/l v. AA: 1·17 (sd 0·18) mmol/l; P= 0·033) and a higher risk of diabetes (OR 3·3, 95 % CI 1·2, 9·2). Combined effects for both SNP increased TAG concentrations by 37 % (P= 0·033). Adherence to the MD modulated the effects of GCKR polymorphism on TAG: subjects with genetic risk had lower TAG (L-allele carriers; PP: 1·48 (sd 0·14) mmol/l v. PL+LL: 1·51 (sd 0·08) mmol/l; P= 0·917) compared with those with a higher adherence. Analysis of the joint effects of the GCKR and individual food items identified significant associations (olive oil (P= 0·035), vegetables (P= 0·012), red meat (P= 0·017), butter (P= 0·039), sweetened carbonated beverages (P= 0·036) and nuts (P= 0·038)). In conclusion, we found that rs1260326 (GCKR) is significantly associated with higher TAG concentrations, but is modulated by adherence to the MD.

Epidemiological studies have demonstrated the benefits of nut consumption on cardiovascular risk factors and CHD, attributed to their fatty acid profile, rich in unsaturated fatty acids, and also to other nutrients. The effect of nuts on atherosclerotic lesions was studied in female and male apoE-knockout mice fed a diet supplemented with 3 % (w/w) mixed nuts (mix: almonds, hazelnuts and walnuts in a proportion of 0·25:0·25:0·50, respectively), and compared with mice receiving an isoenergetic diet of similar fat content provided as palm oil. After 12 weeks, plasma lipid parameters and aortic lesions were measured. Males receiving nuts had lower plasma cholesterol than the palm oil group, and both sex groups had lower plasma non-HDL-cholesterol and lower content of reactive oxygen species in LDL than mice receiving the palm oil diet, the latter decrease being more pronounced in females than in males. Females consuming the nut diet showed a smaller aortic lesion area than those consuming palm oil, whereas no differences were observed in males. In females, hepatic paraoxonase 2 (Pon2) mRNA increased, and no change was observed in prenylcysteine oxidase 1 (Pcyox1) expression after the consumption of the nut-containing diet. In addition, aortic atherosclerotic lesions correlated directly with total plasma cholesterol and inversely with hepatic Pon2 expression. The results suggest that the beneficial effect of nut intake in female apoE-deficient mice may be attributed to reduced non-HDL-cholesterol levels and enhanced PON2 antioxidant activity.

Maslinic acid is found in various natural sources, most notably in pomace olive oil, and exerts pro-apoptotic activities in various cancer cells in vitro. In the present study, DU145 human prostate cancer cells were cultured with 0–25 μm-maslinic acid to examine the effects of maslinic acid on the metastatic capacity of prostate cancer cells. Maslinic acid significantly (P <0·05) inhibited the basal and epidermal growth factor (EGF)-induced migration (27–64 %), invasion (23–60 %) and adhesion (8–40 %) of DU145 cells. Maslinic acid significantly (P <0·05) down-regulated both basal and EGF-stimulated secretion of matrix metalloproteinase (MMP)-9 (25–67 %), MMP-2 (50–86 %), urokinase-type plasminogen activator (uPA, about 100 %), vascular endothelial growth factor (VEGF, 98–100 %) and tissue inhibitors of metalloproteinases (TIMP)-1, as well as expression of uPA receptor (uPAR), intercellular adhesion molecules (22–33 %), vascular cell adhesion molecules (23–46 %) and E-cadherin, whereas it increased TIMP-2 secretion. Maslinic acid dramatically reduced the levels of hypoxia-inducible factor-1α (HIF-1α) protein and mRNA; the reduction was accompanied by reduced stability, nuclear levels and transcriptional activity of HIF-1α. The levels of phospho-Akt and phospho-extracellular signal-related kinase (ERK) were reduced in cells treated with maslinic acid, and the phosphoinositide 3-kinase inhibitor LY294002 and the mitogen-activated protein kinase kinase inhibitor PD98059 reduced HIF-1α levels and VEGF secretion. The results show that maslinic acid markedly inhibited the migration, invasion and adhesion of DU145 prostate cancer cells. Suppressing HIF-1α activation by inhibiting Akt and ERK activation may be part of the mechanism by which maslinic acid inhibited uPAR, E-cadherin, VEGF and MMP expression in DU145 cells.

We investigate the cytoprotective effects and the molecular mechanism of genistein in oxidative stress-induced injury using an endothelial cell line (EA.hy926). An oxidative stress model was established by incubating endothelial cells with H2O2. According to the present results, genistein pretreatment protected endothelial cells against H2O2-induced decreases in cell viability and increases in apoptosis. Genistein also prevented the inhibition of B-cell lymphoma 2 and the activation of caspase-3 induced by H2O2. Genistein increased superoxide dismutase (SOD), catalase (CAT) and glutathione (GSH) levels and attenuated the decrease in these antioxidants during oxidative stress. We also found that genistein induced the promoter activity of both nuclear factor erythroid 2-related factor 2 (Nrf2) and PPARγ. Additionally, genistein induced the nuclear translocation of Nrf2 and PPARγ. While genistein caused the up-regulation of both Nrf2 and PPARγ, it also activated and up-regulated the protein expression and transcription of a downstream protein, haem oxygenase-1 (HO-1). Moreover, the use of Nrf2 small interfering RNA transfection and HO-1- or PPARγ-specific antagonists (Znpp and GW9662, respectively) blocked the protective effects of genistein on endothelial cell viability during oxidative stress. Therefore, we conclude that oxidative stress-induced endothelial cell injury can be attenuated by treatment with genistein, which functions via the regulation of the Nrf2 and PPARγ signalling pathway. Additionally, the endogenous antioxidants SOD, CAT and GSH appear to play a role in the antioxidant activity of genistein. The present findings suggest that the beneficial effects of genistein involving the activation of cytoprotective antioxidant genes may represent a novel strategy in the prevention and treatment of cardiovascular endothelial damage.

Malnutrition in early life impairs glucose-stimulated insulin secretion in adulthood. Conversely, pregnancy is associated with a significant increase in glucose-stimulated insulin secretion under conditions of normoglycaemia. A failure in β-cell adaptive changes may contribute to the onset of diabetes. Thus, glucose homeostasis and β-cell function were evaluated in control-fed pregnant (CP) and non-pregnant (CNP) or protein-restricted pregnant (LPP) and non-pregnant (LPNP) rats, from fetal to adult life, and in protein-restricted rats that were recovered after weaning (RP and RNP). The typical insulin resistance of pregnancy was not observed in the RP rats, nor did pregnancy increase the insulin content/islet in the LPP group. The glucose dose–response curves from pregnant rats were shifted to the left in relation to the non-pregnant rats, except in the recovered group. Glucose utilisation but not oxidation in islets from the RP and LPP groups was reduced at a concentration of 8·3 mm-glucose compared with islets from the CP group. Cyclic AMP content and the potentiation of glucose-stimulated insulin secretion by isobutylmethylxanthine at a concentration of 2·8 mm-glucose indicated increased adenylyl cyclase 3 activity but reduced protein kinase A-α activity in islets from the RP and LPP rats. Protein kinase C (PKC)-α but not phospholipase C (PLC)-β1 expression was reduced in islets from the RP group. Phorbol-12-myristate 13-acetate produced a less potent stimulation of glucose-stimulated insulin secretion in the RP group. Thus, the alterations exhibited by islets from the LPP group appeared to be due to reduced islet mass and/or insulin biosynthesis. In the RP group the loss of the adaptive capacity apparently resulted from uncoupling between glucose metabolism and the amplifying signals of the secretory process, as well as a severe attenuation of the PLC/PKC pathway.

A total of 364 female Ross 308 chicks (1 d old) were used in the present study conducted in floor pens to investigate the effects of graded levels of supplementary bacterial phytase on dietary energy utilisation and growth performance. For this purpose, four maize–soyabean-based diets were offered to the birds from 0 to 21 d of age. These included a suboptimal P negative control (NC, 3·0 g/kg non-phytate P), NC+250 phytase units (FTU)/kg feed, NC+500 FTU and NC+2500 FTU. The effect of phytase activity on bird growth performance was best described as a linear relationship between increasing dose and increased feed intake (P< 0·001), but was quadratic for body-weight gain (P= 0·002) and feed efficiency (P= 0·023). There was no significant response (P>0·05) of dietary apparent metabolisable energy (AME) to supplementary phytase. The birds fed phytase increased their retention of total carcass energy in a linear fashion (P= 0·009) with increased phytase dose. The efficiency of dietary AME used for overall carcass energy retention also improved (P= 0·007) in a linear manner with increased dietary phytase activity. Dietary net energy for production (NEp) increased (P= 0·047) with an increase in phytase dose following a linear pattern, as an increase of 100 FTU increased dietary net energy by 15·4 J (estimated within the range of doses used in the present experiment). Dietary NEp was more highly correlated with performance criteria than dietary AME, and it seems to be a more sensitive way to evaluate broiler response to phytase supplementation.

Salecan is a recently identified water-soluble viscous extracellular β-1,3-d-glucan polysaccharide from an Agrobacterium species. It is a high-molecular-mass polymer (about 2 × 106Da) and composed of a linear chain of glucosyl residues linked through a repeat unit of seven β-(1,3) and two α-(1,3) glucosidic bonds. In the present study, we examined the effects of dietary Salecan fed at 2 and 5 % in a high-fat diet (64 % energy) in C57BL/6J mice. After 6 weeks, mice fed 2 and 5 % Salecan had significantly lower body weight, fat mass and percentage of body fat mass compared with those fed a high-fat cellulose (control) diet. Both the Salecan groups significantly and dose-dependently improved glucose tolerance, with a 9 and 26 % reduction of glucose AUC, respectively. Liver and adipose tissue weights were also significantly decreased by the Salecan treatment. Supplementation with 5 % Salecan led to lower serum TAG, total cholesterol (TC) and HDL-cholesterol (52, 18 and 19 %, respectively) and lower hepatic TAG by 56 % and TC by 22 % compared with the high-fat cellulose control group. Dietary Salecan intake caused an obvious elevation of fat in the faeces. Supplementation with Salecan disturbed bile acid-promoted emulsification and reduced the size of emulsion droplets in vitro. These results indicate that Salecan decreases fat absorption, improves glucose tolerance and has biologically important, dose-related effects on reducing high-fat diet-induced obesity.

The present study investigated the potential health-promoting effects of heat-inactivated Lactobacillus gasseri TMC0356 (TMC0356) on the metabolic syndrome (MS) and the probable mechanisms underlying these effects using an MS rat model. For the purpose of the study, sixty Sprague–Dawley rats were randomly divided into five groups: a control group fed a conventional diet, an MS model group fed a high-fat and high-salt (HFS) diet and three TMC0356 test groups (low-, medium- and high-dose groups) fed an HFS diet supplemented with TMC0356 at 41·8, 83·5 and 167·0 mg/kg body weight (BW) per d, respectively. Food intake and BW were measured weekly. Fasting blood glucose (FBG), lipid profiles and blood pressure (BP) were measured at 0, 5, 10 and 15 weeks. Organ coefficients, immune cell counts and serum insulin, adiponectin, C-reactive protein (CRP), IL-6, TNF-α, IgG and secretory IgA levels were measured at the 15th week after diet intervention. The HFS diet increased the BW, liver or fat:BW ratio, FBG, homeostatic model assessment of insulin resistance, adiponectin, serum LDL-cholesterol and total cholesterol levels and BP (P< 0·01). Average food and energy intakes in the three TMC0356 groups were significantly lower than those of the MS model group. All the metabolic indices, except BP, were markedly improved (P< 0·05) by oral administration of low and medium doses of TMC0356. The thymus index in the medium-dose group and lymphocyte, CRP, IL-6, TNF-α and IgG levels in all the three TMC0356 groups were significantly increased (P< 0·05 or P< 0·01) compared with those in the MS model group. These results suggest that TMC0356 can improve the metabolic characteristics of MS rats by suppressing appetite. Additionally, the enhancement of inflammatory immune response may be, at least in part, the mechanism underlying the health-promoting effects of TMC0356 on the MS.

Lactating rats reinfected with Nippostrongylus brasiliensis fed low-crude protein (CP) foods show reduced lactational performance and less resistance to parasites compared with their high-CP counterparts. Here, we hypothesised that feeding high-CP foods deficient in specific essential amino acids (AA) would result in similar penalties. Second-parity lactating rats, immunised with 1600 N. brasiliensis infective larvae before mating, were fed foods with either 250 (high protein; HP) or 150 (low protein; LP) g CP/kg, or were HP deficient in either leucine (HP-Leu) or methionine (HP-Met). On day 1 of lactation, litter size was standardised at twelve pups. On day 2, dams were either reinfected with 1600 N. brasiliensis larvae or sham-infected with PBS. Dams and litters were weighed daily until either day 8 or 11, when worm burdens, and inflammatory cells and systemic levels of N. brasiliensis-specific Ig isotypes were assessed. Data from five out of sixteen HP-Met rats were omitted due to very high levels of food refusals from parturition onwards. Relative to feeding HP foods, feeding LP, HP-Met and HP-Leu foods reduced dam weight gain and, to a lesser extent, litter weight gain, and increased the number of worm eggs in the colon, indicative of a reduction in resistance to parasites. However, only feeding LP and HP-Leu foods resulted in increased worm numbers, while none of the feeding treatments affected systemic Ig, mast and goblet cells, and eosinophil numbers. The present results support the view that resistance to parasites during lactation may be sensitive to specific essential AA scarcity.

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

Pharmacological antioxidant vitamins have previously been investigated for a prophylactic effect against exercise-induced oxidative stress. However, large doses are often required and may lead to a state of pro-oxidation and oxidative damage. Watercress contains an array of nutritional compounds such as β-carotene and α-tocopherol which may increase protection against exercise-induced oxidative stress. The present randomised controlled investigation was designed to test the hypothesis that acute (consumption 2 h before exercise) and chronic (8 weeks consumption) watercress supplementation can attenuate exercise-induced oxidative stress. A total of ten apparently healthy male subjects (age 23 (sd 4) years, stature 179 (sd 10) cm and body mass 74 (sd 15) kg) were recruited to complete the 8-week chronic watercress intervention period (and then 8 weeks of control, with no ingestion) of the experiment before crossing over in order to compete the single-dose acute phase (with control, no ingestion). Blood samples were taken at baseline (pre-supplementation), at rest (pre-exercise) and following exercise. Each subject completed an incremental exercise test to volitional exhaustion following chronic and acute watercress supplementation or control. The main findings show an exercise-induced increase in DNA damage and lipid peroxidation over both acute and chronic control supplementation phases (P< 0·05 v. supplementation), while acute and chronic watercress attenuated DNA damage and lipid peroxidation and decreased H2O2 accumulation following exhaustive exercise (P< 0·05 v. control). A marked increase in the main lipid-soluble antioxidants (α-tocopherol, γ-tocopherol and xanthophyll) was observed following watercress supplementation (P< 0·05 v. control) in both experimental phases. These findings suggest that short- and long-term watercress ingestion has potential antioxidant effects against exercise-induced DNA damage and lipid peroxidation.

Weight loss leading to cachexia is associated with poor treatment response and reduced survival in pancreatic cancer patients. We aim to identify indicators that allow for early detection that will advance our understanding of cachexia and will support targeted anti-cachexia therapies. A total of fifty pancreatic cancer patients were analysed for skeletal muscle and visceral adipose tissue (VAT) changes using computed tomography (CT) scans. These changes were related to physical characteristics, secondary disease states and treatment parameters. Overall, patients lost 1·72 (sd 3·29) kg of muscle and 1·04 (sd 1·08) kg of VAT during the disease trajectory (413 (sd 213) d). After sorting patients into tertiles by rate of VAT and muscle loss, patients losing VAT at > − 0·40 kg/100 d had poorer survival outcomes compared with patients with < − 0·10 kg/100 d of VAT loss (P= 0·020). Patients presenting with diabetes at diagnosis demonstrated significantly more and accelerated VAT loss compared with non-diabetic patients. In contrast, patients who were anaemic at the first CT scan lost significantly more muscle tissue and at accelerated rates compared with non-anaemic patients. Accelerated rates of VAT loss are associated with reduced survival. Identifying associated features of cachexia, such as diabetes and anaemia, is essential for the early detection of cachexia and may facilitate the attenuation of complications associated with cachexia.

The present study evaluated, using a well-controlled dehydration protocol, the effects of 24 h fluid deprivation (FD) on selected mood and physiological parameters. In the present cross-over study, twenty healthy women (age 25 (se 0·78) years) participated in two randomised sessions: FD-induced dehydration v. a fully hydrated control condition. In the FD period, the last water intake was between 18.00 and 19.00 hours and no beverages were allowed until 18.00 hours on the next day (23–24 h). Water intake was only permitted at fixed periods during the control condition. Physiological parameters in the urine, blood and saliva (osmolality) as well as mood and sensations (headache and thirst) were compared across the experimental conditions. Safety was monitored throughout the study. The FD protocol was effective as indicated by a significant reduction in urine output. No clinical abnormalities of biological parameters or vital signs were observed, although heart rate was increased by FD. Increased urine specific gravity, darker urine colour and increased thirst were early markers of dehydration. Interestingly, dehydration also induced a significant increase in saliva osmolality at the end of the 24 h FD period but plasma osmolality remained unchanged. The significant effects of FD on mood included decreased alertness and increased sleepiness, fatigue and confusion. The most consistent effects of mild dehydration on mood are on sleep/wake parameters. Urine specific gravity appears to be the best physiological measure of hydration status in subjects with a normal level of activity; saliva osmolality is another reliable and non-invasive method for assessing hydration status.

Nutritional evaluation may predict clinical outcomes, such as hospital length of stay (LOS). We aimed to assess the value of nutritional risk and status methods, and to test standard anthropometry percentiles v. the 50th percentile threshold in predicting LOS, and to determine nutritional status changes during hospitalisation and their relation with LOS. In this longitudinal prospective study, 298 surgical patients were evaluated at admission and discharge. At admission, nutritional risk was assessed by Nutritional Risk Screening-2002 (NRS-2002), Malnutrition Universal Screening Tool (MUST) and nutritional status by Subjective Global Assessment (SGA), involuntary % weight loss in the previous 6 months and anthropometric parameters; % weight loss and anthropometry were reassessed at discharge. At admission, risk/undernutrition results by NRS-2002 (P< 0·001), MUST (P< 0·001), % weight loss (P< 0·001) and SGA (P< 0·001) were predictive of longer LOS. A mid-arm circumference (MAC) or a mid-arm muscle circumference (MAMA) under the 15th and the 50th percentile, which was considered indicative of undernutrition, did predict longer LOS (P< 0·001); conversely, there was no association between depleted triceps skinfold (TSF) and longer LOS. In-hospital, there was a high prevalence of weight, muscle and fat losses, associated with longer LOS. At discharge, patients with a simultaneous negative variation in TSF+MAC+MAMA (n 158, 53 %) had longer LOS than patients with a TSF+MAC+MAMA positive variation (11 (8–15) v. 8 (7–12) d, P< 0·001). We concluded that at risk or undernutrition evaluated by all methods, except TSF and BMI, predicted a longer LOS. Moreover, MAC and MAMA measurements and their classification according to the 50th percentile threshold seem reliable undernutrition indicators.

Previous studies on individual foods and nutrients and Parkinson's disease (PD) risk have been inconsistent. Furthermore, only one study has examined the association between the quality of diet and PD. We investigated the prediction of food groups and diet quality on PD in the Finnish Mobile Clinic Survey (1966–72). The population comprised 4524 individuals, aged 40–79 years and free from PD at baseline. Data collection included health examinations, a questionnaire and a 1-year dietary history interview. A modified Alternate Healthy Eating Index was formed to assess diet quality. Statistical analyses were based on Cox's model. During a 41-year follow-up, eighty-five incident cases of PD occurred. No statistically significant associations were found between PD incidence and most of the food groups examined. A few exceptions were fruits and berries in men and milk in women, which showed positive associations. An inverse association between the intake of meat products and PD was found in women. The diet quality index did not predict PD, the adjusted relative risk between the highest and lowest quartiles being 1·83 (95 % CI 0·65, 5·18) in men and 0·97 (95 % CI 0·38, 2·48) in women. The present study suggests that since most of the single food groups or the quality of diet did not predict PD occurrence, the role of diet is apparently rather modest.

Because of its strong association (r 0·85) with percentage of body fat determined by dual-energy X-ray absorptiometry, hip circumference divided by height1·5 (the body adiposity index) has recently been proposed as an index of body fatness among adults. We examined whether this proposed index was more strongly associated with skinfold thicknesses and levels of CVD risk factors (lipids, fasting insulin and glucose, and blood pressure) than was BMI among 2369 18- to 49-year-olds in the Bogalusa Heart Study. All analyses indicated that the body adiposity index was less strongly associated with skinfold thicknesses and CVD risk factors than was either waist circumference or BMI. Correlations with the skinfold sum, for example, were r 0·81 (BMI) v.r 0·75 (body adiposity index) among men, and r 0·87 (BMI) v.r 0·80 among women; P< 0·001 for both differences. An overall index of seven CVD risk factors was also more strongly associated with BMI (r 0·58) and waist circumference (r 0·61) than with the body adiposity index (r 0·49). The weaker associations with the body adiposity index were observed in analyses stratified by sex, race, age and year of examination. Multivariable analyses indicated that if either BMI or waist circumference were known, the body adiposity index provided no additional information on skinfold thicknesses or risk factor levels. These findings indicate that the body adiposity index is likely to be an inferior index of adiposity than is either BMI or waist circumference.

Hmong are one of the immigrant Asian subgroups with increasing rates of obesity, type 2 diabetes and CVD. Despite their population growth in the USA and declining health status, no research has investigated the appropriateness of dietary assessment measures, including FFQ and 24 h dietary recalls among Hmong. The present study compared the nutrient information obtained through a 24 h dietary recall method with that collected using the Block Kid's Food Frequency Questionnaire (Block FFQ) among Hmong-American children (n 335) of 9–18 years of age. For this purpose, two 24 h dietary recalls were collected during non-consecutive days and averaged for comparison. The Block FFQ was administered on the day of the second 24 h recall and the two methodologies were also compared using t tests. Among all children, Block FFQ nutrient estimates for vitamin A, vitamin C and food group servings for vegetables and fruits were significantly higher than those assessed through the 24 h dietary recalls (P< 0·001). Nutrient estimates for protein and food group servings for grains and meat and beans were significantly higher among all participants when assessed through the 24 h dietary recalls than through the Block FFQ (P< 0·05). The results suggest that the Block FFQ does not appear to be a good measure of protein, grain, and meat and bean intake among Hmong children of 9–18 years of age, and the 24 h dietary recall offers a better account of the Hmong diet and is inclusive of ethnic food options otherwise missed in the Block FFQ. We recommend the modification of the current Block FFQ to appropriately reflect cultural food/beverage items of the population in interest.

Fish consumption is the major dietary source of EPA and DHA, which according to rodent experiments may reduce body fat mass and prevent obesity. Only a few human studies have investigated the association between fish consumption and body-weight gain. We investigated the association between fish consumption and subsequent change in body weight. Women and men (n 344 757) participating in the European Prospective Investigation into Cancer and Nutrition were followed for a median of 5·0 years. Linear and logistic regression were used to investigate the associations between fish consumption and subsequent change in body weight. Among women, the annual weight change was 5·70 (95 % CI 4·35, 7·06), 2·23 (95 % CI 0·16, 4·31) and 11·12 (95 % CI 8·17, 14·08) g/10 g higher total, lean and fatty fish consumption per d, respectively. The OR of becoming overweight in 5 years among women who were normal weight at enrolment was 1·02 (95 % CI 1·01, 1·02), 1·01 (95 % CI 1·00, 1·02) and 1·02 (95 % CI 1·01, 1·04) g/10 g higher total, lean and fatty consumption per d, respectively. Among men, fish consumption was not statistically significantly associated with weight change. Adjustment for potential over- or underestimation of fish consumption did not systematically change the observed associations, but the 95 % CI became wider. The results in subgroups from analyses stratified by age or BMI at enrolment were not systematically different. In conclusion, the present study suggests that fish consumption has no appreciable association with body-weight gain.

In the interpretation of dietary trends, it is important to consider the potential effect of modifications in the dietary assessment method. Therefore, our objective was to explore the comparability of data obtained at two time points by a semi-quantitative FFQ (SFFQ) which has had slight modifications over time. In the national dietary surveys among Norwegian 2-year-olds, diet was assessed by an SFFQ which underwent modifications between the 1999 survey and the 2007 survey. In the present study, fifty-nine families with a 2-year-old child participated by completing both the SFFQ in a crossover design within a month's time. With regard to the reported intake of energy and nutrients, the largest significant differences observed between the two questionnaires were for carbohydrates and added sugar. According to intake of food groups, significant differences were observed for five out of sixteen food groups. Spearman's correlation coefficients for energy, nutrients and food groups ranged from 0·43 (Ca) to 0·85 (soft drinks). Most Bland–Altman plots indicated broad limits of agreement. The differences between the two questionnaires can be explained by changes in the questionnaires, changes in the food composition databases used and random variation. Comparing differences between the questionnaires by maternal educational level, number of children and type of day care revealed minor differences. In conclusion, this study showed that at the group level there was reasonable comparability between the two questionnaires, except for carbohydrates, added sugar and some food groups. Moreover, there were moderate to high correlations for energy, nutrients and food groups.

We studied the association, and its direction, between the introduction of solids and weight-for-height (WFH) change between birth and 45 months. Pregnant women were asked to participate in a birth cohort during their first antenatal visit. Data from 3184 children were used. The timing of the introduction of solids was reported by the mother from a questionnaire at 12 months postpartum, and categorised into very early (0–3 months), early (3–6 months) and timely (after 6 months) introduction of solids. Anthropometric data were collected during standardised child health centre visits. WFH was converted into a z-score. Repeated-measurements analyses with splines positioned according to the moments of solid introduction were used to obtain estimates for WFH change before and after the introduction of solids. Analyses were adjusted for educational level, ethnicity, smoking during pregnancy, mother's BMI, breast-feeding, history of food allergy and infant's hospital admission. Before solids were introduced, weight gain was higher in children introduced to solids early (z= 0·65, 95 % CI 0·34, 0·95) than in children introduced to solids very early (z= 0·02, 95 % CI − 0·03, 0·08) and timely (z= − 0·04, 95 % CI − 0·05, − 0·03). Shortly after the introduction of solids, children introduced to solids very early and early showed a relative decrease in WFH. WFH change did not differ between the solid introduction groups after 12 months, and at that time, weight change was as expected (i.e. z= 0). We therefore conclude that differences in WFH in childhood are not the result of early introduction to solids.