Fe deficiency in women contributes significantly to maternal and child morbidity in India. The intestinal bacterial flora may facilitate absorption of Fe from the caecum and proximal colon. The present study investigated the possibility that intestinal microbiota of anaemic young women may differ from that of women with normal Hb levels. The microbiota was quantified by real-time PCR in faeces of eight anaemic (Hb ≤ 100 g/l) and twenty-six normohaemic (Hb ≥ 120 g/l) women aged 18–25 years. Sequences of 16S ribosomal DNA (rDNA) specific to Bifidobacterium genus, Lactobacillus acidophilus group, Bacteroides–Prevotella–Porphyromonas group, Clostridium leptum group and Eubacterium rectale were amplified and expressed (as relative difference) relative to the universally conserved bacterial 16S rDNA sequences. Dietary intakes of energy, carbohydrate, fibre and Fe were ascertained by maintenance of a diet diary for a week. Faecal lactobacilli were significantly lower in anaemic women (median 6·6 × 10− 8, relative difference compared with total bacteria) than in the reference group (2·9 × 10− 6; P = 0·001, unpaired t test with logarithmic transformation). There was no difference between the two groups with respect to any of the other bacteria that were examined. Intakes of energy, carbohydrate, fibre, Fe and milk were similar in both the groups. Fe deficiency in young women in south India was associated with low levels of lactobacilli in the faeces. The relationship between lactobacilli and Fe deficiency needs to be explored further.

Metabolic programming and metabolic imprinting describe early life events, which impact upon on later physiological outcomes. Despite the increasing numbers of papers and studies, the distinction between metabolic programming and metabolic imprinting remains confusing. The former can be defined as a dynamic process whose effects are dependent upon a critical window(s) while the latter can be more strictly associated with imprinting at the genomic level. The clinical end points associated with these phenomena can sometimes be mechanistically explicable in terms of gene expression mediated by epigenetics. The predictivity of outcomes depends on determining if there is causality or association in the context of both early dietary exposure and future health parameters. The use of biomarkers is a key aspect of determining the predictability of later outcome, and the strengths of particular types of biomarkers need to be determined. It has become clear that several important health endpoints are impacted upon by metabolic programming/imprinting. These include the link between perinatal nutrition, nutritional epigenetics and programming at an early developmental stage and its link to a range of future health risks such as CVD and diabetes. In some cases, the evidence base remains patchy and associative, while in others, a more direct causality between early nutrition and later health is clear. In addition, it is also essential to acknowledge the communication to consumers, industry, health care providers, policy-making bodies as well as to the scientific community. In this way, both programming and, eventually, reprogramming can become effective tools to improve health through dietary intervention at specific developmental points.

The Hyperglycemia and Adverse Pregnancy Outcome (HAPO) study of over 23 000 diabetes-free pregnancies has shown that at a population level an unequivocal linear relationship exists between maternal glucose concentrations around the beginning of the third trimester of pregnancy and the risk of their baby being born above the ninetieth centile for weight. With the rising incidence of gestational diabetes (GDM) across the developed world, largely paralleling the increased prevalence of obesity, there has been a sharp increase in the risk of pregnancy complications developing related to the birth of macrosomic babies. The associated additional long-term complications of GDM pregnancies means that in the future there is likely to be a large increase in the incidence of type 2 diabetes and associated conditions in both the mothers and their affected offspring. The present review seeks to highlight recent advances and remaining gaps in knowledge about GDM in terms of its genetics (where some of the recently discovered polymorphic risk factors for type 2 diabetes have also proved to be risk factors for GDM) and its treatment by diet, exercise and drugs.

The ability of nuts to improve the blood lipid profile and reduce the risk of CHD is now well established. The interest that health effects of nuts have gained recently has brought the possible benefits of consuming nuts, such as improvement in the conditions of the metabolic syndrome, and their potential to prevent and control diabetes into focus. Results from cohort studies have associated nut consumption with a reduced risk of developing diabetes and CVD. However, few randomised controlled trials have assessed the effect of nuts on diabetes control, and those that have been undertaken have shown improvements in blood lipids but not in the glycaemic control. Diabetes agencies are increasingly recognising the importance of controlling postprandial glycaemia fluctuations. Acute feeding studies indicate that nuts have minimal effects on rising postprandial blood glucose levels when eaten alone, and diminish the postprandial glycaemic response when consumed with high-glycaemic index carbohydrate foods in both normoglycaemic and type 2 diabetic individuals. Nuts have a healthy nutritional profile, high in MUFA and PUFA, are a good source of vegetable protein and are rich in fibre, vitamins and minerals. Incorporation of nuts in the diet may therefore improve the overall nutritional quality of the diet. While more research is required to establish the ability of nuts to improve glycaemic control in the long run, early data indicate that the inclusion of nuts in the diets of individuals with diabetes and the metabolic syndrome is warranted, in view of their potential to reduce CHD risk.

Prevalence of hypovitaminosis D in Western populations is high; pregnant women are identified as a high-risk group, especially if dark skinned. Consequences of severe clinical vitamin D deficiency in pregnancy can be life threatening to the newborn, while lesser degrees of hypovitaminosis D may have important long-term implications for offspring health. Past experiences with routine provision of 10 μg/d (400 IU/d) to all pregnant mothers suggest that this dose is sufficient to prevent overt neonatal complications of vitamin D deficiency. Recent data suggest that supplementation with dosages above 10 μg/d may be required for optimal health in the mother and child; however, further research is required for the assessment of the benefits and safety of supplementation with higher dosages. Lack of unified advice on vitamin D supplementation of pregnant mothers in the UK hinders the implementation of primary prevention strategies and is likely to leave some deficient mothers without supplementation.

There is some evidence for a nutritional interaction between vitamin D and vitamin K status. We have recently reported that serum percentage undercarboxylated osteocalcin (%ucOC; a marker of vitamin K status) was inversely correlated with serum 25-hydroxyvitamin D (25(OH)D) concentration (reflective of vitamin D status) in healthy Danish girls (aged 11–12 years), in line with a similar relationship reported in elderly women. While the causal nature of the relationship between vitamin D status and serum %ucOC has been tested in studies of elderly women, it has not been investigated in children. The objective of the present study was to test the hypothesis that improving vitamin D status significantly lowers serum %ucOC. Serum samples from sixty-seven healthy Danish girls (aged 11–12 years), who participated in a 12-month double-blind, placebo-controlled, vitamin D3 intervention trial were used for the present study. These girls were a subset of subjects which began and finished the intervention during wintertime, thus avoiding the influence of seasonality on vitamin D status. A total of thirty-three and thirty-four of the girls had been randomised to treatment with 10 μg vitamin D3 per d and placebo, respectively, for 12 months. Total osteocalcin and the fraction of ucOC in serum (via enzyme-immunoassay) as well as serum 25(OH)D (via HPLC) were assessed at baseline and end-point. Vitamin D3 supplementation significantly increased serum 25(OH)D (21·6 %; P < 0·002) but had no effect on serum %ucOC (P>0·8). In conclusion, the findings of the present intervention study in young girls suggest that vitamin D supplementation does not affect serum %ucOC, a marker of vitamin K status.

The different compartments of the gastrointestinal tract are inhabited by populations of micro-organisms. By far the most important predominant populations are in the colon where a true symbiosis with the host exists that is a key for well-being and health. For such a microbiota, ‘normobiosis’ characterises a composition of the gut ‘ecosystem’ in which micro-organisms with potential health benefits predominate in number over potentially harmful ones, in contrast to ‘dysbiosis’, in which one or a few potentially harmful micro-organisms are dominant, thus creating a disease-prone situation. The present document has been written by a group of both academic and industry experts (in the ILSI Europe Prebiotic Expert Group and Prebiotic Task Force, respectively). It does not aim to propose a new definition of a prebiotic nor to identify which food products are classified as prebiotic but rather to validate and expand the original idea of the prebiotic concept (that can be translated in ‘prebiotic effects’), defined as: ‘The selective stimulation of growth and/or activity(ies) of one or a limited number of microbial genus(era)/species in the gut microbiota that confer(s) health benefits to the host.’ Thanks to the methodological and fundamental research of microbiologists, immense progress has very recently been made in our understanding of the gut microbiota. A large number of human intervention studies have been performed that have demonstrated that dietary consumption of certain food products can result in statistically significant changes in the composition of the gut microbiota in line with the prebiotic concept. Thus the prebiotic effect is now a well-established scientific fact. The more data are accumulating, the more it will be recognised that such changes in the microbiota's composition, especially increase in bifidobacteria, can be regarded as a marker of intestinal health. The review is divided in chapters that cover the major areas of nutrition research where a prebiotic effect has tentatively been investigated for potential health benefits. The prebiotic effect has been shown to associate with modulation of biomarkers and activity(ies) of the immune system. Confirming the studies in adults, it has been demonstrated that, in infant nutrition, the prebiotic effect includes a significant change of gut microbiota composition, especially an increase of faecal concentrations of bifidobacteria. This concomitantly improves stool quality (pH, SCFA, frequency and consistency), reduces the risk of gastroenteritis and infections, improves general well-being and reduces the incidence of allergic symptoms such as atopic eczema. Changes in the gut microbiota composition are classically considered as one of the many factors involved in the pathogenesis of either inflammatory bowel disease or irritable bowel syndrome. The use of particular food products with a prebiotic effect has thus been tested in clinical trials with the objective to improve the clinical activity and well-being of patients with such disorders. Promising beneficial effects have been demonstrated in some preliminary studies, including changes in gut microbiota composition (especially increase in bifidobacteria concentration). Often associated with toxic load and/or miscellaneous risk factors, colon cancer is another pathology for which a possible role of gut microbiota composition has been hypothesised. Numerous experimental studies have reported reduction in incidence of tumours and cancers after feeding specific food products with a prebiotic effect. Some of these studies (including one human trial) have also reported that, in such conditions, gut microbiota composition was modified (especially due to increased concentration of bifidobacteria). Dietary intake of particular food products with a prebiotic effect has been shown, especially in adolescents, but also tentatively in postmenopausal women, to increase Ca absorption as well as bone Ca accretion and bone mineral density. Recent data, both from experimental models and from human studies, support the beneficial effects of particular food products with prebiotic properties on energy homaeostasis, satiety regulation and body weight gain. Together, with data in obese animals and patients, these studies support the hypothesis that gut microbiota composition (especially the number of bifidobacteria) may contribute to modulate metabolic processes associated with syndrome X, especially obesity and diabetes type 2. It is plausible, even though not exclusive, that these effects are linked to the microbiota-induced changes and it is feasible to conclude that their mechanisms fit into the prebiotic effect. However, the role of such changes in these health benefits remains to be definitively proven. As a result of the research activity that followed the publication of the prebiotic concept 15 years ago, it has become clear that products that cause a selective modification in the gut microbiota's composition and/or activity(ies) and thus strengthens normobiosis could either induce beneficial physiological effects in the colon and also in extra-intestinal compartments or contribute towards reducing the risk of dysbiosis and associated intestinal and systemic pathologies.

Human milk oligosaccharides, representing the third largest fraction of human milk, have been assigned important protective functions for newborns acting as bifidogenic substrates or as inhibitory agents towards pathogens. Using high-pH anion-exchange chromatography and an enzyme test kit, twenty oligosaccharides and lactose were determined in milk samples of German women from days 3 to 90 postpartum. Twenty-two secretor mothers with Lewis blood group Le(a − b+) synthesised all twenty oligosaccharides, and could be assigned to milk group 1. Five non-secretor mothers (Le(a+b − )) produced all oligosaccharides with the exception of α1,2-fucosylated compounds (milk group 2), whereas three secretor mothers with blood type Le(a − b − ) lacked α1,4-fucosyloligosaccharides, corresponding to milk group 3. Secretor women of milk groups 1 and 3 synthesised significantly higher amounts of total neutral oligosaccharides and of several total core structures (e.g. lacto-N-tetraose) than non-secretor women. Generally, these oligosaccharides significantly decrease during the first 3 months postpartum. By comparing fucosyloligosaccharides within and among the three milk groups, insight into their biosynthesis could be gained. Six acidic oligosaccharides without fucose residues were detected in milk samples of all mothers. Regression analysis confirmed that total acidic oligosaccharides declined threefold during the study period. Milk samples corresponding to the three milk groups exhibited significant qualitative and quantitative differences during the first 3 months of lactation. It can be assumed that particularly milk of non-secretor women (milk group 2) exerts a modified biological protection in the babies in comparison with milks of secretors (groups 1 and 3).

Infant birth weight has increased in Ireland in recent years along with levels of childhood overweight and obesity. The present article reviews the current literature on maternal glycaemia and the role of the dietary glycaemic index (GI) and its impact on pregnancy outcomes. It is known that maternal weight and weight gain significantly influence infant birth weight. Fetal macrosomia (birth weight >4000 g) is associated with an increased risk of perinatal trauma to both mother and infant. Furthermore, macrosomic infants have greater risk of being obese in childhood, adolescence and adulthood compared to normal-sized infants. There is evidence that there is a direct relationship between maternal blood glucose levels during pregnancy and fetal growth and size at birth, even when maternal blood glucose levels are within their normal range. Thus, maintaining blood glucose concentrations within normal parameters during pregnancy may reduce the incidence of fetal macrosomia. Maternal diet, and particularly its carbohydrate (CHO) type and content, influences maternal blood glucose concentrations. However, different CHO foods produce different glycaemic responses. The GI was conceived by Jenkins in 1981 as a method for assessing the glycaemic responses of different CHO. Data from clinical studies in healthy pregnant women have documented that consuming a low-GI diet during pregnancy reduces peaks in postprandial glucose levels and normalises infant birth weight. Pregnancy is a physiological condition where the GI may be of particular relevance as glucose is the primary fuel for fetal growth.

There is increasing evidence that the postprandial state is an important contributing factor to chronic disease. The role of fruit phenolic compounds to protect health and lower disease risk through their actions in mitigating fed-state metabolic and oxidative stressors is of interest and the topic of the present paper. Two main questions are posed: first, what is the role of plant foods, specifically fruits rich in complex and simple phenolic compounds in postprandial metabolic management; and second, does the evidence support consuming these fruits with meals as a practical strategy to preserve health and lower risk for disease? This review provides an overview of the postprandial literature, specifically on the effect of fruits and their inherent phenolic compounds in human subjects on postprandial lipaemia, glycaemia/insulinaemia and associated events, such as oxidative stress and inflammation. Among the identified well-controlled human trials using a postprandial paradigm, >50 % of the trials used wine or wine components and the remaining used various berries. Notwithstanding the need for more research, the collected data suggest that consuming phenolic-rich fruits increases the antioxidant capacity of the blood, and when they are consumed with high fat and carbohydrate ‘pro-oxidant and pro-inflammatory’ meals, they may counterbalance their negative effects. Given the content and availability of fat and carbohydrate in the Western diet, regular consumption of phenolic-rich foods, particularly in conjunction with meals, appears to be a prudent strategy to maintain oxidative balance and health.

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.

Licorice extracts are known to exhibit anti-carcinogenic activities. However, chronic licorice consumption can lead to serious side effects due to the presence of considerable quantities of glycyrrhizin, which causes severe hypokalaemia and hypertension. In the present study, we evaluated the effects of a hexane–ethanol extract of Glycyrrhiza uralensis (HEGU), which lacks glycyrrhizin, on the metastatic characteristics of DU145 prostate cancer cells. HEGU inhibited basal and epidermal growth factor-induced cell migration, invasion and adhesion in a dose-dependent fashion. HEGU significantly suppressed the secretion and activation of the matrix metalloproteinase (MMP)-2 and MMP-9. The secretion of tissue inhibitor of metalloproteinase (TIMP)-1 was reduced, but that of TIMP-2 was increased in HEGU-treated cells. HEGU reduced the protein levels of integrin-α2, the intercellular adhesion molecule, and the vascular cell adhesion molecule. An active fraction of HEGU was separated via column chromatography, and the structure of the active component, licoricidin, was identified via 1H NMR and 13C NMR. The treatment of DU145 cells with licoricidin induced a reduction in cell migration and the secretion of MMP-9, TIMP-1, urokinase-type plasminogen activator and vascular endothelial growth factor, as well as in the expression of adhesion molecules. These results indicate that HEGU, which contains licoricidin, is a potent anti-metastatic agent, which can markedly inhibit the metastatic and invasive capacity of malignant prostate cancer cells. The observed reductions in the activation of proteases and the levels of adhesion molecules may constitute a component of the mechanisms by which HEGU inhibits the migration and adhesion of prostate cancer cells.

Predicting the magnitude and rate of weight gain for a given increase of energy intake requires a model of whole-body energy expenditure that includes the energy cost of tissue deposition. Here, I introduce a mathematical framework for modelling energy expenditure that elucidates conceptual problems with the classical Kielanowski method for estimating the efficiencies of body fat and protein deposition. An alternative approach uses the theoretical biochemical efficiencies for protein and fat synthesis in combination with models of energy expenditure that include body fat and protein turnover costs. I illustrate this alternative approach using a simple mathematical model applied to previously published data from growing rats and human infants and compare the simple model results with the classical Kielanowski model. While both models fit the data reasonably well (R2>0·87 in rats and R2>0·67 in infants), the Kielanowski method resulted in parameter estimates that varied widely across experiments, had poor precision, and occasionally produced efficiency estimates greater than 1. In contrast, the new method provided precise parameter values and revealed consistencies across different experiments. The proposed mathematical framework has implications for interpreting studies of animal nutrition as well as providing a roadmap for future modelling efforts.

The aim of the present study was to determine the effects of a 6-month dietary vitamin E (VE) deficiency on DNA methylation and gene expression in rat liver. Two enzymes, 5-α-steroid reductase type 1 (SRD5A1) and the regulatory subunit of γ-glutamylcysteinyl synthetase (GCLM), which are differentially expressed on the mRNA level, were analysed for promoter methylation in putative cytosine-phospho-guanine (CpG) island regions located at the 5′ end using base-specific cleavage and matrix-assisted laser desorption ionisation time-of-flight MS. A twofold increase in the mRNA level of SRD5A1 gene and a twofold decrease in the mRNA level of GCLM gene in VE-deficient animals were not associated with different CpG methylation of the analysed promoter region. Furthermore, global DNA methylation was not significantly different in these two groups. Thus, the present results indicate that the VE-induced regulation of SRD5A1 and GCLM in rat liver is not directly mediated by changes in promoter DNA methylation.