The aim of the present study was to analyse the sequence variability of the porcine Zip4-like Zn transporter gene and the association of identified sequence variants with average daily gain, apparent Zn absorption, plasma Zn concentration and Zn concentration in the liver and pancreas. For the purpose of the study, two different sample sets were used. Set one, which was used for sequencing and association analysis, included mRNA from intestinal tissue from thirty-five piglets of a feeding trial. Sample set two consisted of forty-six samples of genomic DNA from sperm or tissue of wild boars and several pig breeds and was used to genotype animals of different breeds. The sequence analysis of porcine Zip4-like complementary DNA in sample set one revealed the presence of seven nucleotide substitutions. Of these, six were synonymous, whereas a substitution of A with C in exon IX (XM_001925360 c.1430A>C) causes an amino acid exchange from glutamic acid to alanine (p.Glu477Ala). The association analysis revealed no influence of the six synonymous substitutions on Zn values, but the non-synonymous nucleotide exchange significantly increased Zn concentration in the pancreas and apparent Zn absorption of the piglets in week 2 of the feeding trial. The parentage of the piglets and the genotyping results in sample set two suggest a breed-specific presence of the A allele in Piétrain for this amino acid substitution. These results indicate that genotype influences the Zn absorption abilities of individual animals, which should be taken into consideration in animal breeding as well as for the selection of experimental animals.

The present study investigated the effects of xanthophyll supplementation on production performance, antioxidant capacity (measured by glutathione peroxidase, superoxide dismutase (SOD), catalase, total antioxidant capacity (T-AOC), and reduced glutathione:oxidised glutathione ratio (GSH:GSSG)) and lipid peroxidation (measured by malondialdehyde (MDA)) in breeding hens and chicks. In Expt 1, 432 hens were fed diets supplemented with 0 (control group), 20 or 40 mg xanthophyll/kg diet. Blood samples were taken at 7, 14, 21, 28 and 35 d of the trial. Liver and jejunal mucosa were sampled at 35 d. Both xanthophyll groups improved serum SOD at 21 and 28 d, serum T-AOC at 21 d and liver T-AOC, and serum GSH:GSSG at 21, 28 and 35 d and liver GSH:GSSG. Xanthophylls also decreased serum MDA at 21 d in hens. Expt 2 was a 2 × 2 factorial design. Male chicks hatched from 0 or 40 mg in ovo xanthophyll/kg diet of hens were fed a diet containing either 0 or 40 mg xanthophyll/kg diet. Liver samples were collected at 0, 7, 14 and 21 d after hatching. Blood samples were also collected at 21 d. In ovo-deposited xanthophylls increased antioxidant capacity and decreased MDA in the liver mainly within 1 week after hatching. Maternal effects gradually vanished during 1–2 weeks after hatching. Dietary xanthophylls increased antioxidant capacity and decreased MDA in the liver and serum mainly from 2 weeks onwards. Data suggested that xanthophyll supplementation enhanced antioxidant capacity and reduced lipid peroxidation in different tissues of hens and chicks.

The risk of colorectal cancer (CRC) may be influenced by aberrant DNA methylation and altered nucleotide synthesis and repair, possibly caused by impaired dietary folate intake as well as by polymorphic variants in one-carbon metabolism genes. A case–control study using seventy-one CRC patients and eighty unrelated healthy controls was carried out to assess the genetic association of fifteen SNP and one insertion in nine genes belonging to the folate pathway. Polymorphism selection was based on literature data, and included those which have a known or suspected functional impact on cancer and missense polymorphisms that are most likely to alter protein function. Genotyping was performed by real-time PCR and PCR followed by restriction analysis. The likelihood ratio statistic indicated that most of the polymorphisms were not associated with the risk of CRC. However, an increased risk of CRC was observed for two variant alleles of SNP mapping on the transcobalamin 2 gene (TCN2): C776G (rs1801198) and c.1026-394T>G (rs7286680). Considering the crucial biological function played by one-carbon metabolism genes, further investigations with larger cohorts of CRC patients are needed in order to confirm our preliminary results. These preliminary results indicate that TCN2 polymorphisms can be a susceptibility factor for CRC.

Fish oil supplementation during pregnancy has been associated with lower levels of cord blood IL-13, suggesting that the administration of n-3 fatty acids may attenuate the development of allergic disease. The present study aimed to investigate the mechanism by which n-3 fatty acid administration influences the production of IL-13. Pregnant BALB/c mice were fed nutritionally complete high-fat diets (15 %, w/w) with an n-3 fatty acid-enriched (DHA 1 %, w/w) or control diet (0 % DHA) immediately following delivery. Pups were exposed during suckling and weaned to the maternal diet for the remainder of the study. The production of IL-13, IL-4, IL-10 and interferon-γ from the splenocytes of ovalbumin (ova)-sensitised animals was assessed following in vitro ova stimulation or unstimulated conditions. Human T helper type 2 (Th2) cells were mitogen-stimulated in the presence or absence of DHA (10 μm) and assessed for IL-13 and IL-4 expression using intracellular flow cytometry. The influence on transcriptional activation was studied using a human IL-13 promoter reporter construct and electromobility shift assay. Ova-activated splenocytes from DHA-fed mice produced less IL-13 (57·2 (se 21·7) pg/ml) and IL-4 (7·33 (se 3·4) pg/ml) compared with cells from the animals fed the control diet (161·5 (se 45·0), P< 0·05; 33·2 (se 11·8), P< 0·05). In vitro, DHA inhibited the expression of IL-13 protein from human Th2 cells as well as transcriptional activation and binding of the transcription factors cyclic AMP response element binding and activating transcription factor 2 to the human IL-13 promoter. These data indicate the potential of n-3 fatty acids to attenuate IL-13 expression, and suggest that they may subsequently reduce allergic sensitisation and the development of allergic disease.

Casein glycomacropeptide (CGMP), a glycoprotein originating during cheese manufacture, has shown promising effects by promoting the growth of some beneficial bacteria in vitro, although its activity has not been well explored. The present study was designed to evaluate the effects of CGMP against enterotoxigenic Escherichia coli (ETEC) K88 in vitro (Trial 1) and in vivo (Trial 2). In Trial 1, increasing concentrations of CGMP (0, 0·5, 1·5 or 2·5 mg/ml) were tested regarding its ability to block the attachment of ETEC K88 to ileal mucosa tissues obtained from piglets. Increasing the concentration of CGMP resulted in a gradual decrease in ETEC K88 attachment to the epithelial surface. In Trial 2, seventy-two piglets were distributed in a 2 × 2 factorial combination including or omitting CGMP in the diet (control diet v. CGMP) and challenged or not with ETEC K88 (yes v. no). Inclusion of CGMP increased crude protein, ammonia and isoacid concentrations in colon digesta. CGMP also increased lactobacilli numbers in ileum and colon digesta, and reduced enterobacteria counts in mucosa scrapings and the percentage of villi with E. coli adherence measured by fluorescence in situ hybridisation. The inclusion of CGMP in the diets of challenged animals also prevented the increase of enterobacteria in ileal digesta. We can conclude that CGMP may improve gut health by diminishing the adhesion of ETEC K88 to the intestinal mucosa, by increasing the lactobacilli population in the intestine and by reducing the overgrowth of enterobacteria in the digestive tract of piglets after an ETEC K88 challenge.

Accurate estimates of lysine requirement are essential to fish feed formulation. However, controversy exists regarding the most appropriate mode to express lysine requirement. In the fish nutrition literature, essential amino acid (AA) requirement has been expressed as a percentage of diet, a percentage of dietary crude protein or a ratio to dietary digestible energy (DE). The controversy lies in the different assumptions regarding the effects of dietary protein and DE on lysine requirement. Non-linear mixed model analysis and multilevel analysis were carried out to investigate whether dietary protein or DE affected lysine requirement of fish. The non-linear mixed model analysis suggests that expressing lysine requirement as a percentage of dietary protein provides a better goodness of fit to the modelling dataset than expressing requirement as a fixed concentration of diet, which in turn is generally better than expressing requirement as a ratio to DE. Results from the multilevel analysis confirm that dietary protein content has a significant effect on lysine requirement, while DE does not. The findings of the present study could contribute to a better understanding of the underlying dietary factors that affect AA requirements of fish. The results of the present study could also be useful for developing nutritional guidelines and feed formulations for fish.

The present study evaluated the potential of affecting amino acid metabolism through intestinal fermentation in domestic cats, using dietary guar gum as a model. Apparent protein digestibility, plasma fermentation metabolites, faecal fermentation end products and fermentation kinetics (exhaled breath hydrogen concentrations) were evaluated. Ten cats were randomly assigned to either guar gum- or cellulose-supplemented diets, that were fed in two periods of 5 weeks in a crossover design. No treatment effect was seen on fermentation kinetics. The apparent protein digestibility (P= 0·07) tended to be lower in guar gum-supplemented cats. As a consequence of impaired small-intestinal protein digestion and amino acid absorption, fermentation of these molecules in the large intestine was stimulated. Amino acid fermentation has been shown to produce high concentrations of acetic and butyric acids. Therefore, no treatment effect on faecal propionic acid or plasma propionylcarnitine was observed in the present study. The ratio of faecal butyric acid:total SCFA tended to be higher in guar gum-supplemented cats (P= 0·05). The majority of large-intestinal butyric acid is absorbed by colonocytes and metabolised to 3-hydroxy-butyrylcoenzyme A, which is then absorbed into the bloodstream. This metabolite was analysed in plasma as 3-hydroxy-butyrylcarnitine, which was higher (P= 0·02) in guar gum-supplemented cats. In all probability, the high viscosity of the guar gum supplement was responsible for the impaired protein digestion and amino acid absorption. Further research is warranted to investigate whether partially hydrolysed guar gum is useful to potentiate the desirable in vivo effects of this fibre supplement.

The amino acid arginine is a well-known growth hormone (GH) stimulator and GH is an important modulator of linear growth. The aim of the present study was to investigate the effect of dietary arginine on growth velocity in children between 7 and 13 years of age. Data from the Copenhagen School Child Intervention Study during 2001–2 (baseline), and at 3-year and 7-year follow-up, were used. Arginine intake was estimated via a 7 d precoded food diary at baseline and 3-year follow-up. Data were analysed in a multilevel structure in which children were embedded within schools. Random intercept and slopes were defined to estimate the association between arginine intake and growth velocity, including the following covariates: sex; age; baseline height; energy intake; puberty stage at 7-year follow-up and intervention/control group. The association between arginine intake and growth velocity was significant for the third and fourth quintile of arginine intake (2·5–2·8 and 2·8–3·2 g/d, respectively) compared with the first quintile ( < 2·2 g/d) (P for trend = 0·04). Protein intake (excluding arginine) was significantly associated with growth velocity; however, the association was weaker than the association between arginine intake and growth velocity (P for trend = 0·14). The results of the present study suggest a dose-dependent physiological role of habitual protein intake, and specifically arginine intake, on linear growth in normally growing children. However, since the study was designed in healthy children, we cannot firmly conclude whether arginine supplementation represents a relevant clinical strategy. Further research is needed to investigate whether dietary arginine may represent a nutritional strategy potentially advantageous for the prevention and treatment of short stature.

Secondary metabolites of herbs and spices are widely used as an alternative strategy in the therapy of various diseases. The polyphenols naringenin, quercetin and curcumin have been characterised as anti-diabetic agents. Conversely, in vitro, naringenin and quercetin are described to inhibit phosphoinositide-3-kinase (PI3K), an enzyme that is essential for the neuronal control of whole body glucose homoeostasis. Using both in vitro and in vivo experiments, we tested whether the inhibitory effect on PI3K occurs in neurons and if it might affect whole body glucose homoeostasis. Quercetin was found to inhibit basal and insulin-induced phosphorylation of Akt (Ser473), a downstream target of PI3K, in HT-22 cells, whereas naringenin and curcumin had no effect. In Djungarian hamsters (Phodopus sungorus) naringenin and quercetin (10 mg/kg administered orally) diminished insulin-induced phosphorylation of Akt (Ser473) in the arcuate nucleus, indicating a reduction in hypothalamic PI3K activity. In agreement with this finding, glucose tolerance in naringenin-treated hamsters (oral) and mice (oral and intracerebroventricular) was reduced compared with controls. Dietary quercetin also impaired glucose tolerance, whereas curcumin was ineffective. Circulating levels of insulin and insulin-like growth factor-binding protein were not affected by the polyphenols. Oral quercetin reduced the respiratory quotient, suggesting that glucose utilisation was impaired after treatment. These data demonstrate that low doses of naringenin and quercetin acutely and potently impair glucose homoeostasis. This effect may be mediated by inhibition of hypothalamic PI3K signalling. Whether chronic impairments in glucose homoeostasis occur after long-term application remains to be identified.

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

An experiment was carried out to study the preventive effect of bacterial meal (BM) produced from natural gas against plant-induced enteropathy in Atlantic salmon (Salmo salar). Salmon were fed a diet based on fish meal (FM) or seven diets with 200 g/kg solvent-extracted soyabean meal (SBM) to induce enteritis in combination with increasing levels of BM from 0 to 300 g/kg. Salmon fed a SBM-containing diet without BM developed typical SBM-induced enteritis. The enteritis gradually disappeared with increasing inclusion of BM. By morphometry, no significant (P>0·05) differences in the size of stretches stained for proliferating cell nuclear antigen were found with 150 g/kg BM compared with the FM diet. Increasing BM inclusion caused a gradual decline in the number of cluster of differentiation 8 α positive (CD8α+) intraepithelial lymphocytes, and fish fed BM at 200 g/kg or higher revealed no significant difference from the FM diet. Histological sections stained with antibody for MHC class II (MHC II) showed that fish with intestinal inflammation had more MHC II-reactive cells in the lamina propria and submucosa, but less in the epithelium and brush border, compared with fish without inflammation. There were no significant (P>0·05) differences in growth among the diets, but the highest levels of BM slightly reduced protein digestibility and increased the weight of the distal intestine. In conclusion, the prevention of SBM-induced enteritis by BM is dose dependent and related to intestinal levels of MHC II- and CD8α-reactive cells.

We have previously described that fish larvae absorb a larger fraction of dietary monoacylglycerol than TAG. To investigate how dietary hydrolysed lipids affect a vertebrate at early life stages over time, we fed Atlantic cod (Gadus morhua) larvae six diets with different degrees of hydrolysed lipids for 30 d. The different diets had no effect on growth, but there was a positive correlation between the level of hydrolysed lipids in the diets and mortality. Important genes in lipid metabolism, such as PPAR, farnesoid X receptor (FXR) and stearoyl-CoA desaturase (SCD), were regulated by the different diets. Genes involved in the oxidative stress response did not respond to the increased lipid hydrolysation in the diets. However, enterocyte damage was observed in animals fed diets with 2·7 % NEFA (diet 3) or more. It is thus possible that mortality was due to infections and/or osmotic stress due to the exposure of the subepithelial tissue. In contrast to earlier experiments showing a positive effect of dietary hydrolysed lipids, we have demonstrated a toxic effect of dietary NEFA on Atlantic cod larvae. Toxicity is not acute but needs time to accumulate.

Public health recommendations do not distinguish between vitamin D2 and vitamin D3, yet disagreement exists on whether these two forms should be considered equivalent. The objective of the present study was to evaluate the effect of a daily physiological dose of vitamin D2 or vitamin D3 on 25-hydroxyvitamin D (25(OH)D) status over the winter months in healthy adults living in Dunedin, New Zealand (latitude 46°S). Participants aged 18–50 years were randomly assigned to 25 μg (1000 IU) vitamin D3 (n 32), 25 μg (1000 IU) vitamin D2 (n 31) or placebo (n 32) daily for 25 weeks beginning at the end of summer. A per-protocol approach, which included ≥ 90 % supplement compliance, was used for all analyses. Serum 25-hydroxyvitamin D3 (25(OH)D3), 25-hydroxyvitamin D2 (25(OH)D2) and parathyroid hormone (PTH) were measured at baseline and at 4, 8, 13 and 25 weeks. Geometric mean total serum 25(OH)D concentrations (sum of 25(OH)D2 and 25(OH)D3) at baseline was 80 nmol/l. After 25 weeks, participants randomised to D2 and placebo had a significant reduction in serum 25(OH)D3 concentrations over the winter months compared with vitamin D3-supplemented participants (both P< 0·001). Supplementation with vitamin D2 increased serum 25(OH)D2 but produced a 9 (95 % CI 1, 17) nmol/l greater decline in the 25(OH)D3 metabolite compared with placebo (P< 0·036). Overall, total serum 25(OH)D concentrations were 21 (95 % CI 14, 30) nmol/l lower in participants receiving vitamin D2 compared with those receiving D3 (P< 0·001), among whom total serum 25(OH)D concentrations remained unchanged. No intervention-related changes in PTH were observed. Daily supplementation of vitamin D3 was more effective than D2; however, the functional consequence of the differing metabolic response warrants further investigation.

Evidence has shown that both C-reactive protein (CRP) and serum amyloid component A (SAA) are increased in individuals with gastritis and stomach cancer. Controlling the level of these biomarkers by inhibiting the gastric infection with high doses of ascorbic acid may reduce the risk of carcinogenesis. A population-based double-blind randomised controlled trial in a Japanese population with atrophic gastritis in an area of high stomach cancer incidence was conducted between 1995 and 2000. Daily doses of 50 or 500 mg vitamin C were given, and 120 and 124 participants completed the 5-year study, respectively. Although serum ascorbic acid was higher in the high-dosage group (1·73 (sd 0·46) μg/l) than in the low-dosage group (1·49 (sd 0·29) μg/l, P< 0·001), at the end of the study, no significant difference was observed for CRP between the low- and high-dosage groups (0·39 (95 % CI 0·04, 4·19) mg/l and 0·38 (95 % CI 0·03, 4·31) mg/l, respectively; P= 0·63) or for SAA between the low- and high-dosage groups (3·94 (95 % CI 1·04, 14·84) μg/ml and 3·85 (95 % CI 0·99, 14·92) μg/ml, respectively; P= 0·61). Vitamin C supplementation may not have a strong effect on reducing infections in individuals with atrophic gastritis.

Non-alcoholic fatty liver disease is associated with insulin resistance and dyslipidaemia and can progress to steatohepatitis and cirrhosis. We sought to determine whether dietary fat and saturated fat content alter liver fat in the absence of weight change in an older population. Liver fat was quantified by magnetic resonance spectroscopy before and after 4 weeks on an isoenergetic low-fat/low-saturated fat/low-glycaemic index (LGI) (LSAT: 23 % fat/7 % saturated fat/GI < 55) or a high-fat/high-saturated fat/high-GI (HSAT: 43 % fat/24 % saturated fat/GI>70) diet in older subjects. In the present study, twenty subjects (seven males/thirteen females; age 69·3 (sem 1·6) years, BMI 26·9 (sem 0·8) kg/m2) were randomised to the LSAT diet and fifteen subjects (six males/nine females; age 68·6 (sem 1·8) years, BMI 28·1 (sem 0·9) kg/m2) to the HSAT diet. Weight remained stable. Liver fat decreased significantly on the LSAT diet (median 2·2 (interquartile range (IQR) 3·1) to 1·7 (IQR 1·8) %, P= 0·002) but did not change on the HSAT diet (median 1·2 (IQR 4·1) to 1·6 (IQR 3·9) %). The LSAT diet lowered fasting glucose and total cholesterol, HDL-cholesterol and LDL-cholesterol and raised TAG (P< 0·05), while the HSAT diet had no effect on glucose or HDL-cholesterol but increased total cholesterol and LDL-cholesterol (P< 0·05). Fasting insulin and homeostasis model of insulin resistance did not change significantly on either diet, but the Matsuda index of insulin sensitivity improved on the LSAT diet (P< 0·05). Assignment to the LSAT v. HSAT diet was a predictor of changes in lipid parameters but not liver fat. We conclude that diet composition may be an important factor in the accumulation of liver fat, with a low-fat/low-saturated fat/LGI diet being beneficial.

To determine the effects of length of gestation and sex on infant body composition, air displacement plethysmography was performed in forty-six full-term neonates at 3 d of life and during the week prior to hospital discharge in 180 preterm neonates. Fat mass, as a percentage of body weight, was higher in preterm than in term infants (13·4 (sd 4·2) v. 10·1 (sd 3·7) %, respectively; P= 0·001). The absolute amount of fat mass did not differ between preterm and full-term newborns (323 (sd 126) v. 335 (sd 138) g; P= 0·58), whereas lean body mass was lower in preterm than in term infants (2055 (sd 280) v. 2937 (sd 259) g, respectively; P< 0·001). Among full-term infants, fat mass was higher in females than in males (11·1 (sd 3·7) v. 9·0 (sd 3·3) %, respectively; P= 0·047), whereas we did not observe any sex difference in preterm infants (13·5 (sd 4·1) v. 13·4 (sd 4·3) %; P= 0·89). Our data suggest that by the time they are discharged from hospital: (1) preterm infants have a higher percentage of body fat than term neonates and (2) this is presumably due to a lesser accretion in lean body mass in the first few weeks of extra-uterine life, particularly in boys.

Iodine deficiency has re-emerged in many parts of the world including the UK, Australia and New Zealand (NZ). In 2009, the NZ government introduced the mandatory fortification of bread with iodised salt as a strategy to improve iodine intakes. The aim of the present study was to assess the impact of fortification on the iodine status of NZ schoolchildren. A school-based cluster survey was used to randomly select schools from two NZ cities. Children aged 8–10 years were administered a general questionnaire, and asked to provide a casual urine and finger-prick blood sample. The median urinary iodine concentration (UIC) of the children (n 147) was 113 μg/l, which falls between 100 and 199 μg/l indicating adequate iodine status; 12 % of children had a UIC < 50 μg/l and 39 % had a UIC < 100 μg/l. The median serum thyroxine concentration was 115 nmol/l. The median serum thyroglobulin (Tg) concentration was 10·8 μg/l and falls in the 10·0–19·9 μg/l range indicative of mild iodine deficiency, suggesting that these children still had enlarged thyroid glands. When compared with the median UIC of 68 μg/l reported in the 2002 NZ Children's Nutrition Survey, the UIC of children in the present study had increased, which is probably caused by the addition of iodised salt to bread. However, the elevated concentration of Tg in these children suggests that the increase in UIC is not sufficient to ensure that thyroid volume has normalised. The fortification of other staple foods, in addition to bread, should be considered to ensure good iodine status in NZ children.

A number of studies suggest that breast-feeding has beneficial effects on an individual's cardiovascular risk factors in adulthood, although the mechanisms involved are unknown. One possible explanation is that adults who were breastfed differ in their health behaviours. In a historical cohort, adult health behaviours were examined in relation to type of milk feeding in infancy. From 1931 to 1939, records were kept on all infants born in Hertfordshire, UK. Their type of milk feeding was summarised as breastfed only, breast and bottle-fed, or bottle-fed only. Information about adult health behaviours was collected from 3217 of these men and women when they were aged 59–73 years. Diet was assessed using an administered FFQ; the key dietary pattern was a ‘prudent’ pattern that described compliance with ‘healthy’ eating recommendations. Of the study population, 60 % of the men and women were breastfed, 31 % were breast and bottle-fed, and 9 % were bottle-fed. Type of milk feeding did not differ according to social class at birth, and was not related to social class attained in adult life. There were no differences in smoking status, alcohol intake or reported physical activity according to type of milk feeding, but there were differences in the participants' dietary patterns. In a multivariate model that included sex and infant weight gain, there were independent associations between type of feeding and prudent diet scores in adult life (P= 0·009), such that higher scores were associated with having been breastfed. These data support experimental findings which suggest that early dietary exposures can have lifelong influences on food choice.

Analysis of long-chain n-3 and n-6 fatty acid (FA) concentrations is used to evaluate their potential health effects in epidemiological studies, and, recently, also to counsel patients with a suboptimal intake of n-3 FA. Data on the method's ability to track and detect differences within and between individuals in appropriate populations are, however, lacking. The present study provides such data for twenty-nine plasma phospholipid (PL) FA concentrations and indices measured in 214 newly diagnosed type 2 diabetic patients at baseline and after 3 years. 20 : 3n-6 and the 20 : 4n-6:20 : 3n-6 ratio showed the highest tracking coefficients (Spearman's r 0·68), while DHA, EPA and PLN3-index (EPA+DHA) coefficients were 0·60, 0·47 and 0·55, respectively. Fish consumption measured simultaneously with EPA, DHA, sum n-3 and PLN3 index showed Spearman's correlation coefficients of 0·47, 0·44, 0·48 and 0·49, respectively, decreasing to 0·20, 0·19, 0·22 and 0·21 when measured 3 years apart. The within-subject CV of EPA, DHA and PLN3 index were 39·9, 14·3 and 18·0 %, respectively. The corresponding between-subject CV were 33·6, 16·5 and 18·7 %, while the reference change values were 112, 41 and 52 %. In conclusion, PL n-3 FA concentrations showed a significant long-term tracking and were positively correlated with marine food intake. Analytical precision, biological variability, reference change value and the index of individuality of EPA, DHA and PLN3 index are similar to commonly used clinical biomarkers, supporting their validity as dietary markers in clinical and epidemiological work.

The present cross-sectional study sought to determine the potential relationships between the intake of dairy foods (total dairy products, milk and cheese) and cognitive function through information garnered in the National Health and Nutrition Examination Surveys (1988–94 and 1999–2002). Cognitive measures of vasomotor speed, coding speed and immediate memory recall were assessed from a simple reaction time task (SRTT), symbol–digit substitution test (SDST) and serial digit learning task, respectively, in adults 20–59 years of age. A summation of the percentile rank scores on each of the three tests provided a measure of overall cognitive function. In adults 60 years of age and above, a story recall test and a digit–symbol substitution test (DSST) were utilised to determine cognitive function in an elderly population. The results indicated that cognitive scores for the SRTT were not different between consumers and non-consumers of dairy foods. However, there were associations observed between 20- and 59-year-old consumers of total dairy foods and a higher SDST percentile score (53·2 (se 1·3) to 49·4 (se 2·0)) and a calculated global cognitive percentile score (53·3 (se 1·1) to 50·2 (se 1·4)) compared with non-consumers. A similar significant association was observed with cheese consumers. In adults over 60 years of age, an association between total dairy product consumption and higher DSST percentile scores (51·5 (se 1·9) to 46·2 (se 3·0)) was also observed. These findings highlight the need for additional research on how dairy products may affect cognition and by what mechanisms, through its nutrients or other components.