There is consensus that carbohydrate foods, in the form of fruit, vegetables and whole-grain products, are beneficial to health. However, there are strong indications that highly processed, fibre-depleted, and consequently rapidly digestible, energy-dense carbohydrate food products can lead to over-consumption and obesity-related diseases. Greater attention needs to be given to carbohydrate bioavailability, which is determined by the chemical identity and physical form of food. The objective of the present concept article is to provide a rational basis for the nutritional characterisation of dietary carbohydrates. Based on the properties of carbohydrate foods identified to be of specific relevance to health, we propose a classification and measurement scheme that divides dietary carbohydrates into glycaemic carbohydrates (digested and absorbed in the small intestine) and non-glycaemic carbohydrates (enter the large intestine). The glycaemic carbohydrates are characterised by sugar type, and by the likely rate of digestion described by in vitro measurements for rapidly available glucose and slowly available glucose. The main type of non-glycaemic carbohydrates is the plant cell-wall NSP, which is a marker of the natural fibre-rich diet recognised as beneficial to health. Other non-glycaemic carbohydrates include resistant starch and the resistant short-chain carbohydrates (non-digestible oligosaccharides), which should be measured and researched in their own right. The proposed classification and measurement scheme is complementary to the dietary fibre and glycaemic index concepts in the promotion of healthy diets with low energy density required for combating obesity-related diseases.

The aetiology of CVD is still not completely understood. The present review article summarises data supporting the hypothesis that an insufficient vitamin D status may contribute to the worldwide high prevalence of CVD. Human vitamin D status primarily depends on skin exposure to the UVB spectrum of the sunlight. Epidemiological data indicate that geographic latitude, altitude, season, and the place of residence (urban or rural) are associated with CVD mortality. Interestingly, all these factors also have an influence on human UVB exposure and thus on vitamin D status. Several mechanisms might be responsible for a protective role of vitamin D in CVD. These mechanisms include the inhibition of vascular smooth muscle proliferation, the suppression of vascular calcification, the down regulation of pro-inflammatory cytokines, the up regulation of anti-inflammatory cytokines, and the action of vitamin D as a negative endocrine regulator of the renin–angiotensin system. The first intervention trials indicate that vitamin D may suppress cardiovascular risk markers. However, more controlled clinical trials are needed to investigate whether optimal oral vitamin D supplementation is able to reduce CVD morbidity and mortality.

During fetal life, there are periods of rapid cell proliferation, which are uniquely sensitive to nutritional perturbation. Feeding the pregnant rat a protein-restricted diet alters the growth trajectory of major fetal organs such as the kidney. By day 21 of gestation, the ratio of kidney weight to total body weight is reduced in the fetuses of dams fed a protein-deficient diet. In contrast, the ratio of fetal liver weight to total body weight is unchanged. To investigate the mechanisms underlying this disproportionate change in organ growth in the low-protein group, cell proliferation and differentiation have been assessed in the liver and kidney. The steady-state levels of mRNA for the growth-arrest and DNA-damage gene gadd153/CHOP-10, CCAAT enhancer-binding proteins α and β were unaffected by maternal diet in both fetal liver and kidney. The mRNA for alpha-fetoprotein, albumin and hepatic glucokinase were unchanged in the liver, suggesting that maternal protein deficiency does not alter the state of differentiation. The steady-state levels of the mRNA coding for the cyclin-dependent protein kinase inhibitors (p15INK4a, p19INK4d, p21CIP1, p27KIP1 and p57KIP2) were unchanged in the fetal livers but were significantly increased in the kidneys of fetuses from dams fed the low-protein diet. These results show that the asymmetrical growth of the kidney is associated with increases in mRNA for the Cip/Kip cyclin-dependent kinase inhibitors and that these may reflect specific lesions in organ development.

The WHO recommends exclusive breast-feeding for the first 6 months of life. At present, <2 % of mothers who breast-feed in the UK do so exclusively for 6 months. We propose the testable hypothesis that this is because many mothers do not provide sufficient breast milk to feed a 6-month-old baby adequately. We review recent evidence on energy requirements during infancy, and energy transfer from mother to baby, and consider the adequacy of exclusive breast-feeding to age 6 months for mothers and babies in the developed world. Evidence from our recent systematic review suggests that mean metabolisable energy intake in exclusively breast-fed infants at 6 months is 2·2–2·4 MJ/d (525–574 kcal/d), and mean energy requirement approximately 2·6–2·7 MJ/d (632–649 kcal/d), leading to a gap between the energy provided by milk and energy needs by 6 months for many babies. Our hypothesis is consistent with other evidence, and with evolutionary considerations, and we briefly review this other evidence. The hypothesis would be testable in a longitudinal study of infant energy balance using stable-isotope techniques, which are both practical and valid.

In the current situation where microarray data in the field of nutritional genomics (nutrigenomics) are accumulating rapidly, there is imminent need for an efficient data infrastructure to support research workflow. We have established a web-based, integrated database of the publications and microarray expression data in the field of nutrigenomics. The registered data include links to external databases such as PubMed of the National Center for Biotechnology Information and public microarray databases that contain Minimum Information About a Microarray Experiment-compliant microarray expression data. Using this database, all data sets created will be effectively utilized and shared with other researchers. This database is built on an open-source database system and is freely accessible via the World Wide Web (http://a-yo5.ch.a.u-tokyo.ac.jp/index.phtml</url).

The global profiling of the whole protein complement of the genome expressed in a particular cell or organ, or in plasma or serum, makes it possible to identify biomarkers that respond to alterations in diet or to treatment, and that may have predictive value for the modelling of biological processes. Proteomics has not yet been applied on a large scale in nutritional studies, yet it has advantages over transcriptome profiling techniques in that it directly assesses the entities that carry out the biological functions. The present review summarizes the different approaches in proteomics research, with special emphasis on the current technical ‘workhorses’: two-dimensional (2D)-PAGE with immobilized pH gradients and protein identification by MS. Using a work-flow approach, we provide information and advice on sample handling and preparation, protein solubilization and pre-fractionation, protein separation by 2D-PAGE, detection and quantification via computer-assisted analysis of gels, and protein identification and characterization techniques by means of MS. Examples from nutritional studies employing proteomics are provided to demonstrate not only the advantages but also the limitations of current proteome analysis platforms.

The present review summarizes the results of all published papers on whole-body protein turnover in man measured by [15N]glycine and the end-product method using both urea and ammonia. It begins with a short account of the underlying assumptions and the justification for the use of [15N]glycine. The results are then compared with those of a large sample of measurements by the ‘gold standard’ precursor method with continuous infusion of [13C]leucine. The pros and cons of the two methods are compared and it is suggested that there is a place for further work by the less invasive end-product method, particularly for population studies of the genetic, environmental and functional determinants of whole-body rates of protein synthesis.

Nutrigenomics is the study of how constituents of the diet interact with genes, and their products, to alter phenotype and, conversely, how genes and their products metabolise these constituents into nutrients, antinutrients, and bioactive compounds. Results from molecular and genetic epidemiological studies indicate that dietary unbalance can alter gene–nutrient interactions in ways that increase the risk of developing chronic disease. The interplay of human genetic variation and environmental factors will make identifying causative genes and nutrients a formidable, but not intractable, challenge. We provide specific recommendations for how to best meet this challenge and discuss the need for new methodologies and the use of comprehensive analyses of nutrient–genotype interactions involving large and diverse populations. The objective of the present paper is to stimulate discourse and collaboration among nutrigenomic researchers and stakeholders, a process that will lead to an increase in global health and wellness by reducing health disparities in developed and developing countries.

Particular intestinal bacteria are capable of metabolizing the soya isoflavone daidzein to equol and/or O-desmethylangolensin (O-DMA), and the presence of these metabolites in urine after soya consumption are markers of particular intestinal bacteria profiles. Prevalences of equol producers and O-DMA producers are approximately 30–50 % and 80–90 %, respectively, and limited observations have suggested that these daidzein-metabolizing phenotypes are stable within individuals over time. Characterizing stability of these phenotypes is important to understand their potential as markers of long-term exposure to particular intestinal bacteria and their associations with disease risk. We evaluated concordance within an individual for the equol-producer and O-DMA-producer phenotypes measured at two time points (T1, T2), 1–3 years apart. Phenotypes were ascertained by analysing equol and O-DMA using GC-MS in a spot urine sample collected after 3 d soya (source of daidzein) supplementation. In ninety-two individuals without recent (within 3 months before phenotyping) or current antibiotics use, 41 % were equol producers at T1 and 45 % were equol producers at T2, and 90 % were O-DMA producers at T1 and 95 % were O-DMA producers at T2. The percentage agreement for the equol-producer phenotype was 82 and for the O-DMA-producer phenotype was 89. These results indicate that these phenotypes are stable in most individuals over time, suggesting that they provide a useful biomarker for evaluating disease risk associated with harbouring particular intestinal bacteria responsible for, or associated with, the metabolism of the soya isoflavone daidzein.

Alkylresorcinols, phenolic lipids present in high amounts in whole-grain wheat and rye but not present in appreciable amounts in other foods, are candidates as biomarkers of whole-grain intake from these cereals. We estimated the intake of alkylresorcinols in Sweden and the UK using two different methods: food supply data (FSD); food consumption data (FCD; based on individual and household survey data). The average per capita intake of alkylresorcinols in Sweden was 17·5 mg/d v(FSD) and 22·9 (sd 16·6) mg/d (FCD), while in the UK it was 11·9 mg/d (FSD) and 11·8 (sd 18·62) mg/d (FCD). Ninety-six per cent of all Swedes consumed some alkylresorcinols, compared with 50 % of British people surveyed. Both women and men over the age of 40 years had a higher alkylresorcinol intake than younger people. The average results from the two methods were similar, but the FCD data provided more detail about the range of alkylresorcinol intake, and indicate that because the intake of alkylresorcinols varies so widely, they may be good markers of diets rich or poor in whole-grain wheat/rye products.

Home parenteral nutrition is an established method of supporting patients with intestinal failure, but this treatment may be life long and imposes severe restrictions on daily life. Impact on quality of life is an important outcome when considering the management of home parenteral nutrition patients. This paper reviews studies in which the quality of life of patients receiving home parenteral nutrition has been assessed. A systematic search of electronic databases and relevant publications was undertaken to identify generic or treatment-specific questionnaires used with home parenteral nutrition patients. Many of the thirty-four reports discovered were small studies. Nineteen used non-specific generic instruments, eight used non-validated questionnaires, four used a combination of both, and three did not use any formal tool. Few systematic patterns emerged. There are few available data on the quality of life of home parenteral nutrition patients, and there is a need for standardised, scientifically validated, treatment-specific instruments to measure quality of life in this population.

An optimal diet is one that not only prevents nutrient deficiencies by providing sufficient nutrients and energy for human growth and reproduction, but that also promotes health and longevity and reduces the risk of diet-related chronic diseases. The composition of the optimal diet for women with polycystic ovary syndrome (PCOS) is not yet known, but such a diet must not only assist short term with weight management, symptoms and fertility, but also specifically target the long-term risks of type 2 diabetes, CVD and certain cancers. With insulin resistance and compensatory hyperinsulinaemia now recognised as a key factor in the pathogenesis of PCOS, it has become clear that reducing insulin levels and improving insulin sensitivity are an essential part of management. Diet plays a significant role in the regulation of blood glucose and insulin levels, yet research into the dietary management of PCOS is lacking and most studies have focused on energy restriction rather than dietary composition per se. On the balance of evidence to date, a diet low in saturated fat and high in fibre from predominantly low-glycaemic-index-carbohydrate foods is recommended. Because PCOS carries significant metabolic risks, more research is clearly needed.

The aim of the present study was to investigate the effect of Chinese soft-shelled turtle whole egg powder (TE) on cholesterol metabolism in Sprague–Dawley rats to determine whether it has a cholesterol-lowering effect. Forty male Sprague–Dawley rats were fed a high-fat diet supplemented with TE (0, 0·75, 1·50 or 3·00 g/kg body weight) administrated by gavage for 24 weeks. Serum total cholesterol (TC), HDL-cholesterol (HDL-C), LDL-cholesterol (LDL-C) and faecal total bile acids levels were determined by enzymatic methods. Faecal steroid concentrations were measured by GC. Means and standard deviations were calculated where appropriate for values, and the data were tested by one-way ANOVA. After 24 weeks of feeding a high-fat diet with TE supplementation, serum TC and LDL-C levels, liver cholesterol and liver lipid levels were reduced in rats. TE supplementation did not affect the faecal output, but significantly increased steroid concentrations in faeces, indicating increased steroids excretion. The faecal bile acid excretion was also increased as evidence by elevated mRNA level of liver cytochrome P450, family 7, subfamily A, polypeptide 1. Our results demonstrated that the TE does have a cholesterol-lowering effect by increasing the excretion of total bile acids and neutral steroids.

Enhancement of depressed plasma concentrations of glutamine and arginine is associated with better clinical outcome. Supplementation of glutamine might be a way to provide the patient with glutamine, and also arginine, because glutamine provides the kidney with citrulline, from which the kidney produces arginine when plasma levels of arginine are low. The aim of the present study was to investigate the parenteral and enteral response of the administered dipeptide Ala-Gln, glutamine, citrulline and arginine. Therefore, seven patients received 20 g Ala-Gln, administered over 4 h, parenterally or enterally, on two separate occasions. Arterial blood samples were taken before and during the administration of Ala-Gln. ANOVA and a paired t test were used to test differences (P<0·05). Ala-Gln was undetectable with enteral administration, whereas Ala-Gln remained stable at a plasma concentration of 268 μmol/l throughout parenteral infusion and rapidly decreased towards zero after infusion was stopped. The highest level of glutamine was observed with parenteral infusion of the dipeptide, although enteral infusion also significantly increased plasma levels of glutamine. The highest plasma response of citrulline was observed with the enteral administration of the dipeptide, although parenteral administration also increased plasma levels of citrulline. Plasma arginine increased significantly with parenteral infusion, but not with enteral administration of Ala-Gln. In conclusion, administrations of Ala-Gln, parenteral or enteral, resulted in an increased plasma glutamine response, as compared with baseline. Interestingly, in spite of the high availability of citrulline with enteral administration of the dipeptide, only parenteral infusion of Ala-Gln increased plasma arginine concentration.

The cause of the non-disjunction leading to trisomy 21 remains unclear. Recent evidence has suggested that 5, 10-methylenetetrahydrofolate reductase (MTHFR) and/or methionine synthase reductase (MTRR) might contribute to the maternal risk of trisomy 21. The purpose of the present study was to analyse these findings among the French population and to investigate whether common polymorphisms in genes of the folate and homocysteine pathway, including the MTHFR 677C>T, MTHFR 1298A>C, the methionine synthase (MTR) 2756A>G, the cystathionine β-synthase (CBS) 844Ins68 and the reduced folate carrier (RFC-1) 80G>A polymorphisms, contribute to the risk of trisomy 21. The risk was studied by analysing independent and combined genotypes in 119 case mothers and 119 control mothers. The MTHFR 677T, MTHFR 1298C, MTR2756G, MTRR66G, CBSIns68+ and the RFC-1 80G allele frequencies were not significantly different among French case mothers, compared with control mothers. The risk of having a child with trisomy 21 did not appear to be linked to polymorphisms in genes associated with folate and homocysteine metabolism.

Dietary polyphenols are suggested to participate in the prevention of CVD and cancer. It is essential for epidemiological studies to be able to compare intake of the main dietary polyphenols in populations. The present paper describes a fast method suitable for the analysis of polyphenols in urine, selected as potential biomarkers of intake. This method is applied to the estimation of polyphenol recovery after ingestion of six different polyphenol-rich beverages. Fifteen polyphenols including mammalian lignans (enterodiol and enterolactone), several phenolic acids (chlorogenic, caffeic, m-coumaric, gallic, and 4-O-methylgallic acids), phloretin and various flavonoids (catechin, epicatechin, quercetin, isorhamnetin, kaempferol, hesperetin, and naringenin) were simultaneously quantified in human urine by HPLC coupled with electrospray ionisation mass-MS (HPLC-electrospray-tandem mass spectrometry) with a run time of 6 min per sample. The method has been validated with regard to linearity, precision, and accuracy in intra- and inter-day assays. It was applied to urine samples collected from nine volunteers in the 24 h following consumption of either green tea, a grape-skin extract, cocoa beverage, coffee, grapefruit juice or orange juice. Levels of urinary excretion suggest that chlorogenic acid, gallic acid, epicatechin, naringenin or hesperetin could be used as specific biomarkers to evaluate the consumption of coffee, wine, tea or cocoa, and citrus juices respectively.