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.

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).

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.

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.

Flaxseed is a dietary source of possible chemopreventive compounds such as lignans and α-linolenic acid (ALA). To study the effects of a flaxseed mixture on adenoma formation in multiple intestinal neoplasia mice, the mice were fed a diet containing 2·7 % flaxseed, 4·5 % fibre and 3·7 % ALA. To elucidate the effect of oils of the mixture we also composed a diet without flaxseed but with the same oil composition. The median number of adenomas in the small intestine was fifty-four for the control group, and thirty-seven (P=0·023) and forty-two (P=0·095) for flaxseed and oil groups, respectively. Compared with controls (1·2 mm), the adenoma size was smaller in the flaxseed (0·9 mm; P=0·002) and oil (1·0 mm; P=0·012) groups. Both diets changed the proportions of n-3 and n-6 fatty acids in the colonic mucosa. Membrane β-catenin and protein kinase C (PKC)-ζ levels were reduced in the adenoma v. mucosa (P<0·05), and an inverse association was found between the membrane PKC-ζ in the mucosa and the adenoma number (r −0·460, P=0·008, n 32). Only the flaxseed diet increased lignan levels in the caecum (P=0·002) and in plasma (P=0·002) but they were not associated with tumour formation. The results suggest that the preventive effect of flaxseed on colon carcinogenesis may be due to the oil part of flaxseed, and the loss of β-catenin and PKC-ζ from the membranes of the mucosal tissue may play a permissive role in intestinal tumour development.

Oxysterols are oxygenated derivatives of cholesterol that may be formed endogenously or absorbed from the diet. Significant amounts of oxysterols have frequently been identified in foods of animal origin, in particular highly processed foods. To date, oxysterols have been shown to possess diverse biological activities; however, recent attention has focused on their potential role in the development of atherosclerosis. Oxysterols have been reported to induce apoptosis in cells of the arterial wall, a primary process in the development of atheroma. The aim of the present study was to identify the role of the mitochondria in the apoptotic pathways induced by the oxysterols 7β-hydroxycholesterol (7β-OH) and cholesterol-5β,6β-epoxide (β-epoxide) in U937 cells. To this end, we investigated the effects of these oxysterols on mitochondrial membrane potential, caspase-8 activity, the mitochondrial permeability transition pore and cytochrome c release. 7β-OH-induced apoptosis was associated with a loss in mitochondrial membrane potential after 2 h, accompanied by cytochrome c release from the mitochondria into the cytosol after 16 h. Pre-treatment with a range of inhibitors of the mitochondrial permeability transition pore protected against 7β-OH-induced cell death. In contrast, β-epoxide induced a slight increase in caspase-8 activity but had no effect on mitochondrial membrane potential or cytochrome c release. The present results confirm that 7β-OH-induced apoptosis occurs via the mitochondrial pathway and highlights differences in the apoptotic pathways induced by 7β-OH and β-epoxide in U937 cells.

Raising the dietary PUFA:saturated fatty acids (SFA) ratio has been recommended for the prevention of CVD. However, a high PUFA:SFA (P:S) ratio diet enhances oxidative stress because PUFA are highly susceptible to lipid peroxidation. Thus, we focused on the role of the dietary P:S ratio and peroxidisability index (PI) value on serum and liver tissue and investigated the effects of dietary P:S ratios (0·4, 1·0, and 4·8) with a fixed PI value (81) on serum lipid parameters and hepatic enzyme activities (experiment 1). To elucidate whether those phenomena were unique to the P:S ratio, we examined the effects of dietary PI values (36, 81, 126, and 217) with a constant P:S ratio (1·0) (experiment 2). Female Sprague–Dawley rats weighing 240–280 g were fed experimental diets for 4 weeks. When dietary PI value was maintained at 81, serum HDL-cholesterol (HDL-C) increased with increasing dietary P:S ratio. When the P:S ratio was fixed at 1·0, HDL-C was the lowest with mid–low PI (MLPI) (PI value of 81). In both experiments, serum LDL-cholesterol:HDL-C ratio kept in the range of 0–2. The hepatic superoxide dismutase, catalase, and glutathione peroxidase (GSH-Px) activities and thiobarbituric acid reactive substance (TBARS) concentrations were the highest in the lowest dietary P:S ratio group (experiment 1). GSH-Px, glutathione-S-transferase, and TBARS were the lowest in rats fed the MLPI diet (experiment 2). In conclusion, these results indicate that a P:S ratio of 1·0–1·5 and a PI value of 80–90 in the diet are within a favourable range to reduce the risk of CVD.

Overnourishing the singleton-bearing adolescent sheep throughout pregnancy promotes maternal tissue synthesis at the expense of the nutrient requirements of the gravid uterus. Consequently, the growth of the placenta is impaired and results in the premature delivery of low-birth-weight lambs relative to moderately fed adolescents of equivalent age. To establish if this phenomenon is unique to the growing animal, singleton pregnancies to a single sire were established by embryo transfer into primiparous adult ewes who had attained the normal mature body size for their genotype. Thereafter ewes were offered a maintenance or a high level of a complete diet throughout gestation. High maternal intakes resulted in elevated maternal insulin, no significant change in growth hormone or glucose, and attenuated progesterone and NEFA concentrations. Live weight gain during the first 93 d of gestation was 48 and 244 g/d, and adiposity score at term was 2·4 and 3·7 in the maintenance and high groups, respectively (P<0·001). In spite of achieving levels of adiposity similar to overnourished adolescents, placental (477 (sem 30) v. 518 (sem 41) g) and fetal (5190 (sem 320) v. 5420 (sem 250) g) weights were equivalent in maintenance and high groups. Gestation length was shorter (P<0·01) and colostrum yield at parturition lower (P<0·05) in high v. maintenance dams. Thus, adult sheep appear to be relatively insensitive to the oversupply of nutrients during pregnancy and have the ability to meet the nutrient requirements for normal conceptus growth in spite of their increased adiposity.

The anticarcinogenic effect of vitamin A2 (dehydroretinol and 3-hydroxyretinol) compounds was studied and compared with that of vitamin A1 (retinoic acid, retinol and retinal) and carotenoids (lutein and β-carotene) in the benzo[a]pyrene (B(a)P)-induced forestomach tumour model of female Swiss mice in vivo. Tumour growth and gross tumour incidence observed after the administration of B(a)P (eight doses of 1 mg, twice weekly for 4 weeks) and retinoids/carotenoids (2·5 and 4·7 μm per animal per d, 2 weeks before, during and 2 weeks after B(a)P) showed that the groups supplemented with lutein and 3-hydroxyretinol produced the best results in inhibiting tumour growth and had low tumour incidence compared with the control group given B(a)P only (P<0·05). Weights recorded after the different treatments showed that the β-carotene-supplemented group exhibited maximum weight gain, followed by retinal, retinol, retinoic acid, lutein, dehydroretinol and 3-hydroxyretinol. These results indicate that the anticarcinogenicity of the compounds is not related to the vitamin A biopotencies. Vitamin A2 compounds having half the biopotency of the vitamin A1 compounds were seen to be anticarcinogenic. Again, among the carotenoids, lutein, having 50 % less biopotency, showed more significant results than β-carotene. Thus it is imperative to conclude that the low animal growth achieved with these compounds has a correlation with the highest suppression of tumour occurrence in the present experiment. Therefore, the daily consumption of foods having high content of lutein and vitamin A2 should be given due importance and weight in further studies.

The present study examined: (i) age-induced regional changes in fatty acid composition of brain phospholipids; (ii) α-linolenic acid deficiency-induced regional depletion and recovery of DHA in the brain. DHA and arachidonic acid (AA) did not distribute evenly in the brain. In weaning and adult rats, the region with the highest DHA percentage was the cortex whereas the medulla had the lowest DHA percentage. In the aged rats, both the cortex and cerebellum were the regions with the highest DHA percentage whereas in the neonatal rats, the striatum had the greatest percentage of DHA, and the hypothalamus and hippocampus had the least percentage of DHA. Regarding AA, the hippocampus was the region that had the highest percentage whereas the medulla was the region with the lowest percentage except for the neonatal rats, whose cerebellum, hypothalamus, striatum and midbrain had AA percentage lower than hippocampus and cortex. DHA was not proportionally depleted in various regions of brain when the rats were maintained on an n-3-deficient diet for two generations. The results demonstrated that the cortex, hippocampus, striatum, cerebellum and hypothalamus had DHA depleted by >71 %, whereas the midbrain and medulla had only 64 and 57 % DHA depleted, respectively. The most important observation was that the diet reversal for 12 weeks resulted in complete DHA recovery in all regions except for the medulla where the recovery was only 62 %. It was concluded that the location of DHA, n-3 deficiency-induced DHA depletion and reversibility of DHA deficiency across the brain were region-specific.

In intervention and observational studies, it is necessary to determine the number of blood samples required to estimate the true value of Fe-status measures. The aim of the present study was to determine the number of days for blood sampling required in order to measure the ‘true value’ of five Fe-status parameters in young Fe-depleted women and to investigate the effect of menstrual cycle on these measures. Twelve women (aged 23–30 years), non-anaemic but with low Fe stores, participated in the study. Venous blood samples were collected under standardised conditions on fifteen non-consecutive days during a 5-week period. All blood samples were analysed for Hb, serum ferritin (SF), serum transferrin receptors (sTfR), red blood cell volume distribution width (RDW) and reticulocytes (RET), and body Fe stores were calculated as the ratio between sTfR and SF. No systematic changes were found in the investigated parameters during the study. When analytical variations were accounted for, the day-to-day variations (CV%) were as follows: Hb 2·9 %, SF 8·2 %, RET 26·0 %, RDW 2·4 % and sTfR 8·1 %. Calculating the ‘true value’ with a 5 % significance level and 80 % power showed that one blood sample was sufficient for Hb, SF, sTfR and RDW, whereas seven blood-sampling days were needed for RET. In this study, no significant differences in Fe status were found across the menstrual cycle. The conclusions from this study are valid for studies conducted under similar strict conditions.

Women of childbearing age are at risk of Fe deficiency if insufficient dietary Fe is available to replace menstrual and other Fe losses. Haem Fe represents 10–15 % of dietary Fe intake in meat-rich diets but may contribute 40 % of the total absorbed Fe. The aim of the present study was to determine the relative effects of type of diet and menstrual Fe loss on Fe status in women. Ninety healthy premenopausal women were recruited according to their habitual diet: red meat, poultry/fish or lacto-ovo-vegetarian. Intake of Fe was determined by analysing 7 d duplicate diets, and menstrual Fe loss was measured using the alkaline haematin method. A substantial proportion of women (60 % red meat, 40 % lacto-ovo-vegetarian, 20 % poultry/fish) had low Fe stores (serum ferritin <10 μg/l), but the median serum ferritin concentration was significantly lower in the red meat group (6·8 μg/l (interquartile range 3·3, 16·25)) than in the poultry/fish group (17·5 μg/l (interquartile range 11·3, 22·4) (P<0·01). The mean and standard deviation of dietary Fe intake were significantly different between the groups (P=0·025); the red meat group had a significantly lower intake (10·9 (sd 4·3) mg/d) than the lacto-ovo-vegetarians (14·5 (sd 5·5) mg/d), whereas that of the poultry/fish group (12·8 (sd 5·1) mg/d) was not significantly different from the other groups. There was no relationship between total Fe intake and Fe status, but menstrual Fe loss (P=0·001) and dietary group (P=0·040) were significant predictors of Fe status: poultry/fish diets were associated with higher Fe stores than lacto-ovo-vegetarian diets. Identifying individuals with high menstrual losses should be a key component of strategies to prevent Fe deficiency.

Current research into dietary factors contributing to the development of allergic diseases is directed towards new active approaches instead of passive elimination diets. The present study aimed to investigate the explanatory role of the diet in a probiotic intervention study on the appearance of atopic eczema (AE) in childhood and the safety of perinatal supplementation with probiotics (Lactobacillus rhamnosus strain GG; ATCC 53 103). A prospective follow-up study from birth to 48 months of children (n 159) with a family history of allergic disease was carried out. Outcome measures included growth, dietary intake assessed with 4 d food diaries and their association with AE by logistic regression models. Increased intakes of retinol, Ca and Zn, with perinatal administration of probiotics, reduced the risk of AE, whilst an increase in intake of ascorbic acid increased the likelihood of AE. Perinatal administration of probiotics was safe, as it did not influence the height (mean difference 0·04 (95 % CI −0·33, 0·40) sd scores, P=0·852) or the weight-for-height (mean difference −3·35 (95 % CI −7·07, 0·37)%, P=0·077) of the children at 48 months with and without perinatal administration of probiotics. Up to 48 months, AE did not affect height (mean difference −0·05 (95 % CI −0·42, 0·33) sd scores, P=0·815), but mean weight-for-height in children with AE was −5·1 % (95 % CI −8·9, −1·2 %) lower compared with children without (P=0·010). The joint effects of nutrients and probiotics need to be considered in active prevention and management schemes for allergic diseases.

The polyol isomalt (Palatinit®) is a well established sugar replacer. The impact of regular isomalt consumption on metabolism and parameters of gut function in nineteen healthy volunteers was examined in a randomised, double-blind, cross-over trial with two 4-week test periods. Volunteers received 30 g isomalt or 30 g sucrose daily as part of a controlled diet. In addition to clinical standard diagnostics, biomarkers and parameters currently discussed as risk factors for CHD, diabetes or obesity were analysed. Urine and stool Ca and phosphate excretions were measured. In addition, mean transit time, defecation frequency, stool consistency and weight were determined. Consumption of test products was affirmed by the urinary excretion of mannitol. Blood lipids were comparable in both phases, especially in volunteers with hyperlipidaemia, apart from lower apo A-1 (P=0·03) for all subjects. Remnant-like particles, oxidised LDL, NEFA, fructosamine and leptin were comparable and not influenced by isomalt. Ca and phosphate homeostasis was not affected. Stool frequency was moderately increased in the isomalt phase (P=0·006) without changes in stool consistency and stool water. This suggests that isomalt is well tolerated and that consumption of isomalt does not impair metabolic function or induce hypercalciuria. In addition, the study data indicate that isomalt could be useful in improving bowel function.

The role of bicarbonated mineral waters on lipid metabolism and lipoprotein concentrations in man has scarcely been investigated. The present study aimed to investigate whether drinking sodium bicarbonated mineral water affects postprandial cholesterol and triacylglycerol metabolism in postmenopausal women. In a three-way, randomised, crossover study, eighteen healthy postmenopausal women consumed two sodium bicarbonated mineral waters (bicarbonated mineral water 1 and bicarbonated mineral water 2) and a low mineral water (500 ml of each) with a standard fat-rich meal (4552 kJ; 75·3 g fat). The bicarbonated waters were rich in sodium and bicarbonate and bicarbonated mineral water 1 contained 5·7 times more fluoride than bicarbonated mineral water 2. Fasting blood samples and postprandial blood samples were taken at 30, 60, 120, 240, 360 and 420 min after the end of the meal consumption. Cholesterol and triacylglycerols were determined in serum and chylomicrons. A significant water consumption effect was observed in the total area under the curve (TAUC) of serum and chylomicron triacylglycerols (ANOVA, P=0·008 and P=0·027, respectively). TAUC of serum triacylglycerols for bicarbonated mineral water 2 was significantly lower compared to low mineral water (Bonferroni, P=0·039). Peak concentration of serum triacylglycerols showed a significant water effect (P=0·025). Changes in chylomicron cholesterol were not significantly affected by the type of water. Bicarbonated mineral waters 1 and 2 did not show any significant differences. Drinking sodium bicarbonate-rich mineral waters reduces postprandial lipaemia in healthy postmenopausal women compared to drinking a low mineral water.

Collection of complete and accurate dietary intake data is necessary to investigate the association of nutrient intakes with disease outcomes. A standardised multiple-pass 24 h dietary recall method was used in the International Collaborative Study of Macro- and Micronutrients and Blood Pressure (INTERMAP) to obtain maximally objective data. Dietary interviewers were intensively trained and recalls taped, with consent, for randomly selected evaluations by the local site nutritionist (SN) and/or country nutritionists (CN) using a twelve-criterion checklist marked on a four-point scale (1, retrain, to 4, excellent). In the Belfast centre, seven dietary interviewers collected 932 24 h recalls from 40–59-year-old men and women. Total scores from the 134 evaluated recalls ranged from thirty-four to the maximum forty-eight points. All twelve aspects of the interviews were completed satisfactorily on average whether scored by the SN (n 53, range: probing 3·25 to privacy of interview 3·98) or CN (n 19, range: probing 3·26 to pace of interview and general manner of interviewer 3·95); the CN gave significantly lower scores than the SN for recalls evaluated by both nutritionists (n 31, Wilcoxon signed rank test, P=0·001). Five evaluations of three recalls identified areas requiring retraining or work to improve performance. Reporting accuracy was estimated using BMR; energy intake estimates less than 1·2 × BMR identifying under-reporting. Mean ratios in all age, sex and body-mass groups were above this cut-off point; overall, 26·1 % were below. Experiences from the INTERMAP Belfast centre indicate that difficulties in collection of dietary information can be anticipated and contained by the systematic use of methods to prevent, detect and correct errors.

Strenuous exercise is known to induce oxidative stress leading to the generation of free radicals. The purpose of the present study was to investigate the effects of lycopene, an antioxidant nutrient, at a relatively low dose (2·6 mg/kg per d) and a relatively high dose (7·8 mg/kg per d) on the antioxidant status of blood and skeletal muscle tissues in rats after exhaustive exercise. Rats were divided into six groups: sedentary control (C); sedentary control with low-dose lycopene (CLL); sedentary control with high-dose lycopene (CHL); exhaustive exercise (E); exhaustive exercise with low-dose lycopene (ELL); exhaustive exercise with high-dose lycopene (EHL). After 30 d, the rats in the three C groups were killed without exercise, but the rats in the three E groups were killed immediately after an exhaustive running test on a motorised treadmill. The results showed that xanthine oxidase (XO) activities of plasma and muscle, and muscular myeloperoxidase (MPO) activity in group E were significantly increased compared with group C. Compared with group E, the elevations of XO and MPO activities of muscle were significantly decreased in group EHL. The malondialdehyde concentrations of plasma and tissues in group E were significantly increased by 72 and 114 %, respectively, compared with those in group C. However, this phenomenon was prevented in rats of the ELL and EHL groups. There was no significant difference in the GSH concentrations of erythrocytes in each group; however, exhaustive exercise resulted in a significant decrease in the GSH content of muscle. In conclusion, these results suggested that lycopene protected muscle tissue from oxidative stress after exhaustive exercise.

Evidence suggests that low folate status may be detrimental to mood and associated with depleted cerebrospinal fluid levels of the neurotransmitter serotonin (5-hydroxytryptamine; 5-HT). A placebo-controlled trial was carried out to determine the effect of folic acid supplementation (100 μg for 6 weeks followed by 200 μg for a further 6 weeks) upon subjective mood (Positive and Negative Affect Schedule) and biochemical markers of mood (5-HT) in healthy males (n 23). Blood samples were obtained at baseline (week 0) and during the intervention at week 6 and week 12. Subjective mood assessments were obtained at week 0 and week 12. The results showed an increase in serum and erythrocyte folate concentrations (P=0·02 and P=0·003, respectively) and a corresponding decrease in plasma homocysteine (P=0·015) in response to the folic acid intervention. Neither subjective mood nor 5-HT levels, however, were significantly altered in response to the change in folate status. Folic acid given at physiological doses did not appear to improve the mood of healthy folate-replete individuals over a 12-week period. Further research is needed to address the effect of folic acid supplementation or of longer duration or increased dose, particularly in the face of sub-optimal folate status.

Eating behaviour depends partly on food preference, which is itself determined by different types of emotions. Among the emotions generated by food, disgust with red meat is common in women and can lead to reduced meat consumption. We tested the hypothesis that low meat intake is related to different negative emotions towards meat but does not affect the emotions expressed towards other food categories. Food intake of sixty women was followed throughout each day for 1 week and allowed us to assign women to two groups (low v. high meat-eating women). They were then invited to assess the intensity of twenty-six emotions described by words and induced by thirty food pictures. We determined the number of necessary dimensions to describe the space created by the twenty-six words. The results showed differences in emotions between the low and high meat-eating women. As expected, there were overall differences in the emotions generated by the thirty food pictures. Six clusters of emotions were necessary and sufficient to summarise the emotional space. These dimensions were described by ‘disappointment’, ‘satisfaction’, ‘guilt’, ‘doubt’, ‘amused’ and ‘indifference’. As expected, the low meat-eating women felt more ‘disappointment’, ‘indifference’ and less ‘satisfaction’ towards meat than did the high meat-eating women. However, the low meat-eating women also stated other negative emotions such as ‘doubt’ towards some starchy foods. The only foods that they liked more than high meat-eating women were pears and French beans. In conclusion, low meat consumption was associated with specific negative emotions regarding meat and other foods.