Observational data have suggested that increased water intake decreases the risk of CHD. A postulated mechanism is that increased water ingestion reduces blood viscosity. The aim of the present study was to assess the effect of increased fluid intake on blood viscosity. Men (n 67) and postmenopausal women (n 27) with one or more risk factors for CVD who reported intake of ≤ 0·5 litres water daily were randomised to a control group (n 31), an intervention group (n 32) that increased their daily water intake by 1 litre/d and an intervention group (n 31) that ingested 1 litre blueberry juice/d. All were encouraged to continue their usual diet and lifestyle. Whole-blood viscosity and blood and urine chemistries were measured by standard techniques after 2 and 4 weeks. Urine volume increased (by a median of 872 and 725 ml in the water and blueberry juice groups, respectively, v. 10 ml in the control group; P ≤ 0·002), confirming the subjects' adherence to the protocol. Urine osmolality and urinary levels of Na, K and creatinine decreased in the water and blueberry juice groups v. the controls (P < 0·05). No change was seen in whole-blood viscosity or in levels of fibrinogen, total protein, lipids, glucose, insulin, C-peptide or other chemistry and haematology variables. In conclusion, a postulated protective effect of increased water or fluid intake is not explained by a change in blood viscosity and increased fluid intake does not influence CVD risk factors in the short term.

Weight gain and risk of type 2 diabetes are inversely associated with a high intake of insoluble cereal fibres. Because nutrient-induced changes of ‘satiety hormones’ from the gut may play a role in this process, we evaluated the effects of purified insoluble fibres on postprandial responses of plasma peptide YY (PYY), serum ghrelin and satiety as secondary outcome measures of a study investigating effects of cereal fibres on parameters of glucose metabolism. Fourteen healthy women were studied on six occasions in a randomized, single-blind, controlled crossover design. After 24 h run-in periods and 10 h overnight fasts, subjects ingested isoenergetic and macronutrient matched portions of control white bread or fibre-enriched bread (wheat-fibre or oat-fibre) at 08.15 hours. Gut hormones and hunger scores were measured for 300 min. Basal PYY and ghrelin concentrations were not different between the test meals (P>0·15). Postprandial responses of PYY and ghrelin were blunted after the intake of wheat-fibre (total area under the curve (AUC) PYY, 177·9 (sem 8·1) (pmol/l) min; P=0·016; ghrelin 51·0 (sem 2·5) (pmol/l) min; P=0·003), but not after oat-fibre (PYY 226·7 (sem 25·7) (pmol/l) min; P>0·15; ghrelin 46·2 (sem 1·6) (pmol/l) min; P=0·127), compared to control (PYY 247·5 (sem 25·6) (pmol/l) min; ghrelin 42·5 (sem 1·3) (pmol/l) min). Postprandial hunger scores were unaffected by the different test meals (P>0·15). Thus, oat- and wheat-fibre consumption result in different postprandial responses of PYY and ghrelin, but interestingly do not differ in satiety effects.

There is increasing evidence identifying the crucial role of numerous dietary components in modifying the process of carcinogenesis. The varied effects exerted by nutrient and non-nutrient dietary compounds on human health and cancer risk are one of the new challenges for nutritional sciences. In the present paper, an attempt is made to review the most recent epidemiological data on interactions between dietary factors and metabolic gene variants in terms of cancer risk. The majority of case–control studies indicate the significant relationship between cancer risk and polymorphic xenobiotic metabolising enzymes in relation to dietary components. The risk of colorectal cancer is associated not only with CYP2E1 high-activity alleles, but also GSTA1 low-activity alleles, among consumers of red or processed meat. Genetic polymorphisms of NAT1 and NAT2 may be also a breast-cancer susceptibility factor among postmenopausal women with a high intake of well-done meat. On the other hand, phytochemicals, especially isothiocyanates, have a protective effect against colorectal and lung cancers in individuals lacking GST genes. Moreover, polymorphism of GSTM1 seems to be involved in the dietary regulation of DNA damage. The European Prospective Investigation into Cancer and Nutrition study shows a significant inverse association between the polycyclic aromatic hydrocarbon–DNA adduct level and dietary antioxidants only among GSTM1-null individuals. However, the absence of a modulatory effect of polymorphic xenobiotic metabolising enzymes and diet on the development of cancer has been indicated by some epidemiological investigations. Studies of interactions between nutrients and genes may have great potential for exploring mechanisms, identifying susceptible populations/individuals and making practical use of study results to develop preventive strategies beneficial to human health.

Prevention of retinoic acid-induced craniofacial abnormalities by folinic acid, and endothelin-1 (ET-1)/dHAND protein and mRNA expression were investigated in mouse embryos using the whole embryo culture, streptavidin–biotin peroxidase complex method, and whole-mount in situ hybridization. In the whole embryo culture, 1·0 and 0·1mm-folinic acid dose dependently prevented branchial region malformations and decreased defects by 93% and 77%, respectively. Folinic acid at concentrations of 1·0 and 0·1mm significantly increased ET-1 and dHAND protein expression levels compared to retinoic acid-exposed values in embryonic branchial areas. Folinic acid also increased ET-1 and dHAND mRNA levels in the same region. The present results suggest that folinic acid may prevent retinoic acid-induced craniofacial abnormalities via increasing ET-1 and dHAND levels in the branchial region during the organogenic period.

In countries of the Mediterranean region, nuts have been consumed in moderate quantities since ancient times. Epidemiological studies show lower risk of cardiovascular diseases in populations with frequent nut consumption, independent from other dietary components. This article assesses nut consumption in Spain and other countries using different sources of data collected at the country, household or individual levels. The per capita consumption of nuts in Spain in 2001 was 7·9 g/person/d. The varieties most widely consumed are walnuts, almonds, hazelnuts and peanuts. Results of the eVe study estimate an average nut consumption in the Spanish population aged 25–60 years of 3·3 g/person/d. No significant statistical differences were observed between men and women. Consumption is higher in men aged between 35 and 44 years (4·5 g/d) and in women aged between 45 and 54 years (3·5 g/d). In the population of 2–24 years, according to the enKid study, nut consumption is estimated at 4·9±18·5 g/person per d. The age group with the highest consumption is teenagers between 14 and 17 years. The northeastern, northern and eastern regions of Spain show the highest consumption. According to FAO balance sheets, in 2001, Lebanon (16·5 kg/person peryear) and Greece (11·9 kg/person per year) were the countries in the Mediterranean region with the highest consumption of nuts, followed by Spain (7·3 kg/person per year), Israel and Italy.

The current ecological approach in health behaviour research recognises that health behaviour needs to be understood in a broad environmental context. This has led to an exponential increase in the number of studies on this topic. It is the aim of this systematic review to summarise the existing empirical evidence pertaining to environmental influences on fruit and vegetable (FV) consumption. The environment was defined as ‘all factors external to the individual’. Scientific databases and reference lists of selected papers were systematically searched for observational studies among adults (18–60 years old), published in English between 1 January 1980 and 31 December 2004, with environmental factor(s) as independent factor(s), and fruit intake, vegetable intake or FV intake combined as one outcome measure as dependent factor(s). Findings showed there was a great diversity in the environmental factors studied, but that the number of replicated studies for each determinant was limited. Most evidence was found for household income, as people with lower household incomes consistently had a lower FV consumption. Married people had higher intakes than those who were single, whereas having children showed mixed results. Good local availability (e.g. access to one's own vegetable garden, having low food insecurity) seemed to exert a positive influence on intake. Regarding the development of interventions, improved opportunities for sufficient FV consumption among low-income households are likely to lead to improved intakes. For all other environmental factors, more replicated studies are required to examine their influence on FV intake.

Regulation of energy homeostasis requires precise coordination between peripheral nutrient-sensing molecules and central regulatory networks. Ghrelin is a twenty-eight-amino acid orexigenic peptide acylated at the serine 3 position mainly with an n-octanoic acid, which is produced mainly in the stomach. It is the endogenous ligand of the growth hormone secretagogue (GHS) receptors. Since plasma ghrelin levels are strictly dependent on recent food intake, this hormone plays an essential role in appetite and meal initiation. In addition, ghrelin is involved in the regulation of energy homeostasis. The ghrelin gene is composed of four exons and three introns and renders a diversity of orexigenic peptides as well as des-acyl ghrelin and obestatin, which exhibit anorexigenic properties. Ghrelin stimulates the synthesis of neuropeptide Y (NPY) and agouti-related protein (AgRP) in the arcuate nucleus neurons of the hypothalamus and hindbrain, which in turn enhance food intake. Ghrelin-expressing neurons modulate the action of both orexigenic NPY/AgRP and anorexigenic pro-opiomelanocortin neurons. AMP-activated protein kinase is activated by ghrelin in the hypothalamus, which contributes to lower intracellular long-chain fatty acids, and this appears to be the molecular signal for the expression of NPY and AgRP. Recent data suggest that ghrelin has an important role in the regulation of leptin and insulin secretion and vice versa. The present paper updates the effects of ghrelin on the control of energy homeostasis and reviews the molecular mechanisms of ghrelin synthesis, as well as interaction with GHS receptors and signalling. Relationships with leptin and insulin in the regulation of energy homeostasis are addressed.

Conventional and real-time PCR were used to detect transgenic DNA in digesta, faeces and blood collected from six ruminally and duodenally cannulated sheep fed forage-based (F) or concentrate-based (C) diets containing 15 % Roundup Ready® (RR) rapeseed meal (n 3). The sheep were adapted for 14 d to F or C diets containing non-GM rapeseed, then fed the RR diets for 11 d. On day 12, they were switched back to non-GM diets for a further 11 d. Ruminal and duodenal fluids (RF, DF) and faecal samples were collected at 3 or 4 h intervals over the 4 d immediately following the last feeding of GM diets. DNA was isolated from whole RF and DF, from the cell-free supernatant fraction, and from culture fermentation liquid. Blood was collected on days 1, 5 and 9 of feeding the RR rapeseed meal. The 1363 bp 5-enolpyruvylshikimate-3-phosphate synthase transgene (epsps) was quantifiable in whole RF and DF for up to 13 h, and a 108 bp epsps fragment for up to 29 h. Transgenic DNA was not detectable in faeces or blood, or in microbial DNA. Diet type (F v. C) did not affect (P>0·05) the quantity of transgenic DNA in digesta. More (P < 0·05) transgenic DNA was detected in RF than in DF, but there was an interaction (P < 0·05) between sample type and collection time. In supernatant fractions from RF and DF, three different fragments of transgenic DNA ranging in size from 62 to 420 bp were not amplifiable.

Although progress has been made towards international goals for the eradication of hunger and malnutrition, considerable work is still required to achieve them and to respond to emerging public health nutrition challenges. The present paper outlines sixteen major inter-linked nutrition challenges recently identified by the UN Standing Committee on Nutrition. While many of the challenges relate to the nutritional needs of children and mothers, an increased emphasis on nutrition-related chronic diseases that affect later life is also evident. Promoting healthy ageing and the maintenance of physical and mental function in older age are undoubtedly major challenges for the future, and the present paper also informs on the role of nutrition, specifically n-3 essential fatty acids, in the prevention of cognitive decline. The importance of determining the cost-effectiveness of nutrition interventions is advocated, in order that the nutrition community can respond appropriately to global nutrition challenges.

The precision with which glycaemic responses, expressed as incremental area under the curve (AUC), can be measured may be improved by using the average of several measures of fasting blood glucose (FBG). To see if taking two fasting blood samples would increase the precision of AUC, the glycaemic responses elicited by four test meals (50 g glucose; 50 g glucose plus 10 g fat and 10 g protein; 100 g white bread; 100 g white bread plus 10 g fat and 10 g protein) were determined in thirteen overnight-fasted healthy subjects. Two fasting blood samples were taken 5 min apart (−5 min and 0 min before starting to eat) with glucose measured three times in each sample. AUC was calculated using different estimates of FBG derived from the three measures of glucose in the two fasting blood samples and each set of AUC values subjected to ANOVA. Unexpectedly, the results were more precise when AUC was calculated from mean glucose in the 0 min blood sample (FBG0) than from mean glucose in the two different fasting blood samples. The 95 % CI of the AUC calculated using FBG0 in thirteen subjects was ±29·8; to obtain the same CI using the mean of the two fasting blood samples would require fourteen subjects. These results suggest that taking two fasting blood samples does not necessarily improve, and may even reduce, the precision of AUC as a measure of glycaemic response. Further studies are needed before requiring that two fasting blood samples be taken for determining glycaemic index.

Intake of fibre has beneficial properties on gut health. Butyrate, a product of bacterial gut fermentation, is thought to contribute to positive effects by retarding growth and enhancing apoptosis of tumour cells. One mechanism is seen in its capacity to modulate histone acetylation and thereby transcriptional activity of genes. Next to butyrate, propionate and acetate are also major products of gut fermentation and together they may exert different potencies of cellular effects than butyrate alone. Since virtually nothing is known on combination effects by SCFA mixtures, here we had the aim to assess how physiological relevant concentrations and mixtures of SCFA modulate histone acetylation in human colon cells. HT29 colon cancer cells were incubated with mixtures of butyrate, acetate and propionate and with the individual compounds as controls. Histone acetylation was determined with acid-urea gel electrophoresis and immunoblotting. Acetylated histones slowly increased over 24 h and persisted up to 72 h in butyrate-treated HT29 cells. Butyrate (5–40 mm) and propionate (20–40 mm) enhanced histone acetylation significantly after 24 h incubation, whereas acetate (2·5–80 mm) was ineffective. Mixtures of these SCFA also modulated histone acetylation, mainly due to additive effects of butyrate and propionate, but not due to acetate. In conclusion, physiological concentrations of propionate together with butyrate could have more profound biological activities than generally assumed. Together, these SCFA could possibly mediate important processes related to an altered transcriptional gene activation and thus contribute to biological effects possibly related to cancer progression or prevention.

A number of authors have argued that only an aquatic-based diet can provide the necessary quantity of DHA to support the human brain, and that a switch to such a diet early in hominin evolution was critical to human brain evolution. This paper identifies the premises behind this hypothesis and critiques them on the basis of clinical literature. Both tissue levels and certain functions of the developing infant brain are sensitive to extreme variations in the supply of DHA in artificial feeding, and it can be shown that levels in human milk reflect maternal diet. However, both the maternal and infant bodies have mechanisms to store and buffer the supply of DHA, so that functional deficits are generally resolved without compensatory diets. There is no evidence that human diets based on terrestrial food chains with traditional nursing practices fail to provide adequate levels of DHA or othern-3 fatty acids. Consequently, the hypothesis that DHA has been a limiting resource in human brain evolution must be considered to be unsupported.

Dietary bioactive compounds (vitamin E, carotenoids, polyphenols, vitamin C, Se and Zn) have beneficial effects on skin health. The classical route of administration of active compounds is by topical application direct to the skin, and manufacturers have substantial experience of formulating ingredients in this field. However, the use of functional foods and oral supplements for improving skin condition is increasing. For oral consumption, some dietary components could have an indirect effect on the skin via, for example, secondary messengers. However, in the case of the dietary bioactive compounds considered here, we assume that they must pass down the gastrointestinal tract, cross the intestinal barrier, reach the blood circulation, and then be distributed to the different tissues of the body including the skin. The advantages of this route of administration are that the dietary bioactive compounds are metabolized and then presented to the entire tissue, potentially in an active form. Also, the blood continuously replenishes the skin with these bioactive compounds, which can then be distributed to all skin compartments (i.e. epidermis, dermis, subcutaneous fat and also to sebum). Where known, the distribution and mechanisms of transport of dietary bioactive compounds in skin are presented. Even for compounds that have been studied well in other organs, information on skin is relatively sparse. Gaps in knowledge are identified and suggestions made for future research.

Dietary isoflavones, such as genistein and daidzein, are metabolised by the human gut microflora. Case–control studies have disclosed a link between the formation of the daidzein metabolite equol and prostate cancer risk. We evaluated the effects of genistein, daidzein and five metabolites on two prostate cancer cell lines by determining DNA integrity and cell growth. LNCaP cells contain the T877A androgen receptor mutation whereas Los Angeles prostate cancer (LAPC)-4 cells express the wild-type receptor, both of which may affect responses to isoflavones. DNA integrity was determined using the comet assay. Cell growth was assessed by staining DNA with 4′,6′-diamidino-2-pheylindole hydrochloride. Endogenous steroid hormones, but not isoflavones, induced DNA strand breaks. Dihydrotestosterone stimulated the growth of both cell lines. 17β-Oestradiol increased the growth of LNCaP but not LAPC-4 cells, pointing to an involvement of the T877A androgen receptor. Isoflavones did not stimulate growth in either prostate cancer cell line. However, the growth of LNCaP and LAPC-4 cells was suppressed by genistein (inhibitory concentration 50% (IC50) 39·7μmo/, 37·2μmo/) and by equol (IC50 53·8μmo/, 35·1μmo/). O-desmethylangolensin inhibited the growth of LAPC-4 cells (IC50 45·2μmo/), but not of LNCaP cells. In conclusion, isoflavones do not damage DNA or promote growth of androgen-dependent prostate cancer cells. Several isoflavones, including the reduced daidzein metabolites equol and O-desmethylangolensin, suppress cancer cell growth. Taken together, these data suggest a contribution of gut-formed isoflavone metabolites to the beneficial effects of dietary isoflavones on prostate cancer risk.