Some countries have introduced mandatory folic acid fortification, whereas others support periconceptional supplementation of women in childbearing age. Several European countries are considering whether to adopt a fortification policy. Projections of the possible beneficial effects of increased folic acid intake assume that the measure will result in a considerable reduction in neural-tube defects (NTD) in the target population. Therefore, the objective of the present study is to evaluate the beneficial effects of different levels of folic acid administration on the prevalence of NTD. Countries with mandatory fortification achieved a significant increase in folate intake and a significant decline in the prevalence of NTD. This was also true for supplementation trials. However, the prevalence of NTD at birth declined to approximately five cases at birth per 10 000 births and seven to eight cases at birth or abortion per 10 000 births. This decline was independent of the amount of folic acid administered and apparently reveals a ‘floor effect’ for folic acid-preventable NTD. This clearly shows that not all cases of NTD are preventable by increasing the folate intake. The relative decline depends on the initial NTD rate. Countries with NTD prevalence close to the observed floor may have much smaller reductions in NTD rates with folic acid fortification. Additionally, potential adverse effects of fortification on other vulnerable population groups have to be seriously considered. Policy decisions concerning national mandatory fortification programmes must take into account realistically projected benefits as well as the evidence of risks to all vulnerable groups.

The senescence-accelerated mouse develops normally until 5–6 months of age and then displays rapid and irreversible advancement of senescence manifesting as clinical signs and gross lesions. To clarify the effect of lactic acid bacteria on the physiological changes with increasing age, heat-killed Lactococcus lactis G50 was administered to 1-month-old senescence-accelerated-prone mouse (SAMP)6 mice for 11 months, a senescence-accelerated mouse strain that develops senile osteoporosis. Mice fed G50 gained more weight than the control mice (not fed G50) during the feeding experiment. Faecal IgA levels in the mice fed G50 at 3 months were higher than those of the control mice but decreased to control levels with increasing age. The numbers of viable cells of Bacteroides sp., Lactobacillus sp., Staphylococcus sp., Enterococcus/Streptococcus sp. and Enterobacteriaceae sp. in faeces were similar for mice fed the G50 and control diets at any age, but strain G50 suppressed the intestinal growth of H2S-producing bacteria. Bone density of the thigh bone did not differ between aged G50 and control mice. Strain G50 would be a beneficial bacterium for the enhancement of intestinal immunity during youth and to suppress the growth of harmful intestinal bacteria. The applicability of strain G50 for the food and animal industries has been proposed in the present study.

We aimed to examine the effect of different doses of lutein supplementation on visual function in subjects with long-term computer display light exposure. Thirty-seven healthy subjects with long-term computer display light exposure ranging in age from 22 to 30 years were randomly assigned to one of three groups: Group L6 (6 mg lutein/d, n 12); Group L12 (12 mg lutein/d, n 13); and Group Placebo (maltodextrin placebo, n 12). Levels of serum lutein and visual performance indices such as visual acuity, contrast sensitivity and glare sensitivity were measured at weeks 0 and 12. After 12-week lutein supplementation, serum lutein concentrations of Groups L6 and L12 increased from 0·356 (sd 0·117) to 0·607 (sd 0·176) μmol/l, and from 0·328 (sd 0·120) to 0·733 (sd 0·354) μmol/l, respectively. No statistical changes from baseline were observed in uncorrected visual acuity and best-spectacle corrected visual acuity, whereas there was a trend toward increase in visual acuity in Group L12. Contrast sensitivity in Groups L6 and L12 increased with supplementation, and statistical significance was reached at most visual angles of Group L12. No significant change was observed in glare sensitivity over time. Visual function in healthy subjects who received the lutein supplement improved, especially in contrast sensitivity, suggesting that a higher intake of lutein may have beneficial effects on the visual performance.

The objective of the present study was to analyse whether there is a relationship between the clinical severity at the time of starting transpyloric enteral nutrition (TEN) and the onset of digestive tract complications in critically ill children. Between May 2005 and December 2007, we performed a prospective, observational study with the participation of 209 critically ill children aged between 3 d and 17 years and who received TEN. The characteristics of the nutrition and its tolerance were compared with the paediatric risk of mortality (PRISM), the paediatric index of mortality (PIM) and the paediatric logistic organ dysfunction index (PELOD) at the time of starting the nutrition. Higher PRISM and PELOD scores correlated with a later time of starting enteral nutrition, a longer time to reach the maximum daily energy delivery and a longer duration of the TEN. However, the severity scores did not correlate with the maximum energy delivery achieved. Abdominal distension or excessive gastric residues were observed in 4·7 % of the patients and diarrhoea in 4·3 %. The ability of the severity scores to predict diarrhoea was of 0·67 for PRISM, 0·63 for PELOD and 0·60 for PIM-2.The severity scores were not able to predict other digestive tract complications. Higher scores of clinical severity at the time of starting enteral nutrition correlate with a later initiation of the nutrition, a longer time to reach the maximum energy delivery and a longer duration of TEN. However, their ability to predict digestive tract complications is low.

There has been a growing interest in lignans, a class of phyto-oestrogens, because of their potentially favourable effects on human health. The aim of the present study was to compare the metabolic profile of post-menopausal women consuming various amounts of dietary lignans. Phyto-oestrogen intake was assessed using a 3-d dietary record analysed with a Canadian food phyto-oestrogen content data table in 115 post-menopausal women (age 56·8 (sd 4·4) years and BMI 28·5 (sd 5·9) kg/m2). Plasma enterolactone (ENL), the major biologically active metabolite of dietary lignans, was determined by time-resolved fluoroimmunoassay. Anthropometrics, abdominal adipose tissue areas (computed tomography), body composition (hydrostatic weighing) and insulin sensitivity (hyperinsulinaemic–euglycaemic clamp) were measured in all women. Women in the high dietary lignan intake subgroup (n 29) had a significantly lower BMI and total body fat mass, as well as a better glucose disposal rate (GDR; P < 0·05), compared with women in the low lignan intake subgroup (n 28). The majority of women with the highest dietary lignan intake were also in the highest quartile of plasma ENL (59 %). Women in the highest ENL quartile had a significantly lower BMI (26·1 (sd 4·4) v. 30·4 (sd 6·9) kg/m2, P < 0·05), total body fat mass (24·8 (sd 9·8) v. 33·3 (sd 13·3) kg, P < 0·05), 2 h postload glycaemia (5·5 (sd 0·9) v. 5·7 (sd 0·8) nmol/l, P < 0·05) and a higher GDR (8·3 (sd 2·7) v. 5·5 (sd 2·8), P < 0·01) compared with women in the lowest ENL quartile. In conclusion, women with the highest ENL concentrations had a better metabolic profile including higher insulin sensitivity and lower adiposity measures.

Oligomers and polymers of flavan-3-ols (proanthocyanidins) are very abundant in the Mediterranean diet, but are poorly absorbed. However, when these polyphenols reach the colon, they are metabolised by the intestinal microbiota into various phenolic acids, including phenylpropionic, phenylacetic and benzoic acid derivatives. Since the biological properties of these metabolites are not completely known, in the present study, we investigated the effect of the following microbial phenolic metabolites: 3,4-dihydroxyphenylpropionic acid (3,4-DHPPA), 3-hydroxyphenylpropionic acid, 3,4-dihydroxyphenylacetic acid (3,4-DHPAA), 3-hydroxyphenylacetic acid, 4-hydroxybenzoic acid and 4-hydroxyhippuric acid (4-HHA), on modulation of the production of the main pro-inflammatory cytokines (TNF-α, IL-1β and IL-6). The production of these cytokines by lipopolysaccharide (LPS)-stimulated peripheral blood mononuclear cells (PBMC) pre-treated with the phenolic metabolites was studied in six healthy volunteers. With the exception of 4-HHA for TNF-α secretion, only the dihydroxylated compounds, 3,4-DHPPA and 3,4-DHPAA, significantly inhibited the secretion of these pro-inflammatory cytokines in LPS-stimulated PBMC. Mean inhibition of the secretion of TNF-α by 3,4-DHPPA and 3,4-DHPAA was 84·9 and 86·4 %, respectively. The concentrations of IL-6 in the culture supernatant were reduced by 88·8 and 92·3 % with 3,4-DHPPA and 3,4-DHPAA pre-treatment, respectively. Finally, inhibition was slightly higher for IL-1β, 93·1 % by 3,4-DHPPA and 97·9 % by 3,4-DHPAA. These results indicate that dihydroxylated phenolic acids derived from microbial metabolism present marked anti-inflammatory properties, providing additional information about the health benefits of dietary polyphenols and their potential value as therapeutic agents.

Lycopene β-cyclase (tlcy-b) tomatoes, obtained by modulating carotenogenesis via genetic engineering, contain a large amount of β-carotene, as clearly visible by their intense orange colour. In the present study we have subjected tlcy-b tomatoes to an in vitro simulated digestion and analysed the effects of digestate on cell proliferation. To this aim we used HT-29 human colon adenocarcinoma cells, grown in monolayers, as a model. Digested tomatoes were diluted (20 ml, 50 ml and 100 ml/l) in culture medium and added to the cells for different incubation times (24 h, 48 h and 72 h). Inhibition of cell growth by tomato digestate was dose-dependent and resulted from an arrest of cell cycle progression at the G0/G1 and G2/M phase and by apoptosis induction. A down-regulation of cyclin D1, Bcl-2 and Bcl-xl expression was observed. We also found that heat treatment of samples before digestion enhanced β-carotene release and therefore cell growth inhibition. To induce with purified β-carotene solubilised in tetrahydrofuran the same cell growth inhibition obtained with the tomato digestate, a higher amount of the carotenoid was necessary, suggesting that β-carotene micellarised during digestion is utilised more efficiently by the cells, but also that other tomato molecules, reasonably made available during digestion, may be present and cooperate with β-carotene in promoting cell growth arrest.

Fe deficiency is a public-health problem worldwide, and effective measures for preventing Fe deficiency are needed. The aim of the present study was to determine the bioavailability of Fe in cocoa using the Hb regeneration efficiency (HRE) method. Thirty-five F344/N male weanling rats were fed a low-Fe diet for 4 weeks to deplete body Fe stores. Then, four groups of seven animals each were repleted for 20 d using a modified AIN-93G diet fortified with ferrous sulphate, ferric citrate or two brands of cocoa powder to provide a total dietary Fe concentration of 20 mg/kg. As a negative control, seven rats were maintained on the low-Fe diet. The HRE were 0·733, 0·350, 0·357 and 0·336 for ferrous sulphate, ferric citrate and the two brands of cocoa powder, respectively. The relative biological values (RBV), defined as the ratio of the sample HRE to that of ferrous sulphate, were 0·478, 0·488 and 0·459 for ferric citrate and the two brands of cocoa powder, respectively. The Fe bioavailability of cocoa was significantly less than that of ferrous sulphate and was similar to that of ferric citrate. The difference in Fe bioavailability between the two brands of cocoa powder was negligible. When the negative control was used to correct the data, estimates of the RBV derived from Hb gain were similar to those derived from the HRE. These results suggest that cocoa is a significant source of moderately bioavailable Fe.

Postprandial hyperglycaemia is thought to increase inflammation in leucocytes. In the present study, we examined whether sucrose loading in rats with moderate postprandial hyperglycaemia induces the expression of cytokines in peripheral leucocytes and whether these inductions are suppressed by inhibiting postprandial hyperglycaemia with the α-glucosidase inhibitor miglitol. One group of streptozotocin-treated rats and age-matched saline-treated rats were orally administered sucrose only, and another group of streptozotocin-treated rats was administered sucrose with miglitol, at a single daily dose for 4 d, under 4 h fasting conditions. Blood glucose levels at 0, 0·25, 0·5, 1, 2 and 3 h and cytokine mRNA in peripheral leucocytes at 0 and 3 h after sucrose loading on days 1 and 4 from the start of sucrose loading were determined. Streptozotocin-treated rats showed moderate postprandial hyperglycaemia (>2000 mg/l) at 0·25–1 h after sucrose loading on days 1 and 4. Postprandial hyperglycaemia was not observed in the miglitol-treated rats loaded with sucrose. Gene expression levels of IL-1β and TNF-α were higher in the streptozotocin-treated rats at fasting on day 1 than in saline-treated rats. Fasting IL-1β and TNF-α gene expression on day 1 were not only increased at 3 h on the same day of sucrose loading, but was also increased at the fasting period on day 4. These inductions on day 4 by intermittent sucrose administration were inhibited by miglitol. The present results suggest that miglitol decreases postprandial hyperglycaemia and intermittent sucrose-induced expression of the IL-1β and TNF-α genes in rat peripheral leucocytes.

The present study investigated the effect of dietary Zn deficiency during sexual maturation on sperm integrity and testis phospholipid fatty acid composition. Male weanling Sprague–Dawley rats were randomised into four dietary groups for 3 weeks: Zn control (ZC; 30 mg Zn/kg); Zn marginally deficient (ZMD; 9 mg Zn/kg); Zn deficient (ZD; < 1 mg Zn/kg); pair fed (PF; 30 mg Zn/kg) to the ZD group. Morphology of cauda epididymal sperm and lipid profiles of testis phospholipids were analysed. The rats fed the ZD diet had a lower testis weight (P < 0·02). Seminal vesicles and prostate weight were also lower in the ZD and PF groups. Rats fed the ZD diet, but not the ZMD diet, had 34–35 % more abnormal spermatozoa and 24 % shorter sperm tail length than the ZC and PF rats (P < 0·001). Testis cholesterol concentration was higher in the ZD rats compared with the ZC and PF rats (P < 0·04). Testes were highly enriched with n-6 fatty acids by showing n-6 : n-3 fatty acid ratios of 27:1 in phosphatidylcholine (PC) and 23:1 in phosphatidylethanolamine (PE). The dominant fatty acid in testes was docosapentaenoic acid (22 : 5n-6), comprising 15 and 24 % of PC and PE, respectively. This fatty acid was significantly lower in the ZD rats, whereas 18 : 2n-6 was higher compared with the rats in the other diet groups. These results demonstrate that severe Zn deficiency adversely affects sperm integrity and modulates testis fatty acid composition by interrupting essential fatty acid metabolism. This suggests that Zn deficiency-associated abnormal testicular function is perhaps preceded by altered membrane fatty acid composition, especially of a major fatty acid, 22 : 5n-6.

In recent years the intake of n-6 PUFA and trans-fatty acids (TFA) has increased, whereas n-3 PUFA intake has decreased. The present study investigated the effects of maternal diet high in n-6 PUFA, n-3 PUFA or TFA on glucose metabolism, insulin sensitivity and fatty acid profile in male offspring. Female weanling Wistar/NIN rats were randomly assigned to receive either a diet high in linoleic acid (LA), or α-linolenic acid (ALA), or long-chain n-3 PUFA (fish oil; FO), or TFA, for 90 d, and mated. Upon weaning, pups were randomly divided into seven groups (mother's diet-pup's diet): LA-LA, LA-ALA, LA-FO, ALA-ALA, FO-FO, TFA-TFA and TFA-LA. At the age of 105 d, an oral glucose tolerance test, adipocyte glucose transport and muscle phospholipid fatty acid composition were measured in the pups. All animals displayed normal insulin sensitivity as evidenced by similar plasma insulin and area under the curve of insulin after an oral glucose load. Maternal intake of n-3 PUFA (ALA or FO) resulted in higher n-3 PUFA in the offspring. Plasma cholesterol and NEFA were significantly higher in the TFA-TFA group compared with the other groups. Adipocyte insulin-stimulated glucose transport and adiponectin mRNA expression were lower in TFA-TFA and TFA-LA offspring compared with the other groups. While most mother-pup fatty acid combinations did not influence the measured variables in the pups, these results indicate that maternal intake of TFA led to an unfavourable profile in the pups through to the age of 105 d, whether the pups consumed TFA, or not.

The pharmacokinetics of dietary fucoxanthin, one of the xanthophylls in brown sea algae, is little understood. In the present study, mice were orally administered fucoxanthin, and the distribution and accumulation of fucoxanthin and its metabolites fucoxanthinol and amarouciaxanthin A were measured in the plasma, erythrocytes, liver, lung, kidney, heart, spleen and adipose tissue. In a single oral administration of 160 nmol fucoxanthin, fucoxanthinol and amarouciaxanthin A were detectable in all specimens tested in the present study, but fucoxanthin was not. The time at maximum concentration (Tmax) of these metabolites in adipose tissue was 24 h, while the Tmax in the others was 4 h. The area under the curve to infinity (AUC∞) of fucoxanthinol in the liver was the highest value (4680 nmol/g × h) among the tissues tested in the present study, while the AUC∞ of amarouciaxanthin A in adipose tissue was the highest value (4630 nmol/g × h). In daily oral administration of 160 nmol fucoxanthin for 1 week, fucoxanthin was also detectable in the tissues even at a low concentration. The amount of fucoxanthinol was 123 nmol/g in the heart and 85·2 nmol/g in the liver. Amarouciaxanthin A in the adipose tissue was distributed at a concentration of 97·5 nmol/g. These results demonstrate that dietary fucoxanthin accumulates in the heart and liver as fucoxanthinol and in adipose tissue as amarouciaxanthin A.

Consumption by animals and humans of earthy materials such as clay is often related to gut pathologies. Our aim was to determine the impact of kaolinite ingestion on glucose and NEFA transport through the intestinal mucosa. The expression of hexose transporters (Na/glucose co-transporter 1 (SGLT1), GLUT2, GLUT5) and of proteins involved in NEFA absorption (fatty acid transporter/cluster of differentiation 36 (FAT/CD36), fatty acid transport protein 4 (FATP4) and liver fatty acid binding protein (L-FABP)) was measured (1) in rats whose jejunum was perfused with a solution of kaolinite, and (2) in rats who ate spontaneously kaolinite pellets during 7 and 28 d. Also, we determined TAG and glucose absorption in the kaolinite-perfused group, and pancreatic lipase activity, gastric emptying and intestinal transit in rats orally administered with kaolinite. Glucose absorption was not affected by kaolinite perfusion or ingestion. However, kaolinite induced a significant increase in intestinal TAG hydrolysis and NEFA absorption. The cytoplasmic expression of L-FABP and FATP4 also increased due to kaolinite ingestion. NEFA may enter the enterocytes via endocytosis mainly since expression of NEFA transporters in the brush-border membrane was not affected by kaolinite. After uptake, rapid binding of NEFA by L-FABP and FATP4 could act as an intracellular NEFA buffer to prevent NEFA efflux. Increased TAG hydrolysis and NEFA absorption may be due to the adsorption properties of clay and also because kaolinite ingestion caused a slowing down of gastric emptying and intestinal transit.

Excess calcium is well known to induce iron deficiency. Furthermore, excess calcium increases hepatic copper concentration and decreases renal copper concentration. We investigated the effect of iron supplementation on the tissue distribution of copper in rats given a high-calcium diet. Male rats (5 weeks old) were divided into four groups; a control group, and three groups given a diet containing 5-fold higher calcium than its requirement and an intraperitoneal iron supplementation of 0, 1 or 2 mg/week as iron dextran. The animals were fed their respective experimental diets with or without iron supplementation for 4 weeks. Although the high-calcium diet had no effect on calcium concentrations in the liver, kidney, testis, spleen and plasma, it reduced haematocrit and iron concentrations in the liver, kidney and testis and the rats had a moderate iron deficiency. The iron supplementation restored to normal these signs of iron deficiency. The high-calcium diet increased hepatic copper concentration but decreased plasma copper concentration and ceruloplasmin activity, which was restored by the iron supplementation. The copper concentration in bile was neither affected by the high-calcium diet nor the iron supplementation. The high-calcium diet decreased the copper concentration in the kidney, which was not restored by the iron supplementation. These results suggest that secondary iron deficiency stimulates hepatic accumulation of copper in rats given excess calcium by suppressing copper efflux into the circulation. The reduced renal copper concentration by excess calcium is independent of the iron deficiency.

Previous reports have shown that safflower-seed extract and its major antioxidant constituents, serotonin hydroxycinnamic amides, attenuated atherosclerotic lesion formation in apoE-deficient mice, as well as inflammation and aortic stiffness in human subjects. In the present report, we examined a still unknown cell-based mechanism of serotonin derivatives against the development of atherosclerosis, focusing our attention on their action against the increase of adhesion molecules and the release of chemotactic factors on human aortic endothelial cells, phenomena that represent the key events in the early stages of atherosclerogenesis. Serotonin derivatives N-(p-coumaroyl)serotonin and N-feruloylserotonin exerted an inhibitory effect on short-term high glucose-induced up-regulation of mRNA and protein of adhesion and migration factors, and the consequent adhesion and migration of monocytes to endothelial cells; they inhibited the activation of transcription factors such as NF-κB, and the overproduction of the mitochondrial superoxide by acting as scavengers of the superoxide radical. In addition, serotonin derivative concentration inside the cells and inside the mitochondria was increased in a time-dependent manner. These results identify a mechanism of action of serotonin derivatives against endothelial damage at a cellular level, and underline their benefits against the disorders and complications related to reactive oxygen species.

Riboflavin status is usually measured as the in vitro stimulation with flavin adenine dinucleotide of the erythrocyte enzyme glutathione reductase, and expressed as an erythrocyte glutathione reductase activation coefficient (EGRAC). This method is used for the National Diet and Nutrition Surveys (NDNS) of the UK. In the period between the 1990 and 2003 surveys of UK adults, the estimated prevalence of riboflavin deficiency, expressed as an EGRAC value ≥ 1·30, increased from 2 to 46 % in males and from 1 to 34 % in females. We hypothesised that subtle but important differences in the detail of the methodology between the two NDNS accounted for this difference. We carried out an evaluation of the performance of the methods used in the two NDNS and compared against an ‘in-house’ method, using blood samples collected from a riboflavin intervention study. Results indicated that the method used for the 1990 NDNS gave a significantly lower mean EGRAC value than both the 2003 NDNS method and the ‘in-house’ method (P < 0·0001). The key differences between the methods relate to the concentration of FAD used in the assay and the duration of the period of incubation of FAD with enzyme. The details of the EGRAC method should be standardised for use in different laboratories and over time. Additionally, it is proposed that consideration be given to re-evaluating the basis of the EGRAC threshold for riboflavin deficiency.

Dietary fatty acids (FA) are the major determinants of blood lipids, and measurements of plasma phospholipid FA (PL-FA) composition that reflect the dietary intake of FA may provide insights into the relationships between diet and CHD. We assessed CHD mortality associations with PL-FA (SFA, PUFA and MUFA) levels measured in a nested case–control study of 116 cases of CHD death and 239 controls that were frequency-matched for age and employment grade. The participants had plasma levels of total cholesterol, LDL-cholesterol (LDL-C), HDL-cholesterol, apo B and apo A1, C-reactive protein (CRP) and fibrinogen recorded. SFA levels were significantly positively correlated with total cholesterol, LDL-C, apo B, CRP protein and fibrinogen. By contrast, phospholipid-PUFA were inversely associated with CRP, but not with any of the lipids. A higher SFA content (top v. bottom quarter) was associated with a 2-fold higher risk of CHD (OR and 95 % CI: OR 2·12; 95 % CI: 1·13, 3·99), and an equivalent difference in PUFA was associated with a halving in CHD risk (OR 0·49; 95 % CI: 0·26, 0·94), but MUFA was unrelated to CHD risk. These associations were substantially attenuated, after additional adjustment for lipids and inflammatory markers. Higher levels of saturated fat and lower levels of polyunsaturated fats were each associated with a higher risk of CHD in elderly men, and these associations were partly explained by their effects on blood lipids and biomarkers of inflammation.

To examine the association of plant-based food intakes with CVD and total mortality among Japanese. In the Japan Collaborative Cohort Study for Evaluation of Cancer Risk, 25 206 men and 34 279 women aged 40–79 years, whose fruit, vegetable and bean intakes were assessed by questionnaire at baseline in 1988–90, were followed for 13 years. Deaths from total stroke, stroke subtypes, CHD and total CVD, according to the International Classification for Diseases 10th Revision, were registered. During 756 054 person-years of follow-up, there were 559 deaths from total stroke, 258 from CHD, 1207 from total CVD and 4514 from total mortality for men, and for women, 494, 194, 1036 and 3092, respectively. Fruit intake was inversely associated with mortality from total stroke (the multivariable hazard ratio (HR (95 % CI)) in the highest v. lowest quartiles = 0·67 (0·55, 0·81)), total CVD (HR = 0·75 (0·66, 0·85)) and total mortality (HR = 0·86 (0·80, 0·92)). Vegetable intake was inversely associated with total CVD (HR = 0·88 (0·78, 0·99)). Bean intake was inversely associated with other CVD (HR = 0·79 (0·64, 0·98)), total CVD (HR = 0·84 (0·74, 0·95)) and total mortality (HR = 0·90 (0·84, 0·96)). Further adjustment for other plant-based foods did not alter the association of fruit intake with mortality from total stroke, total CVD and total mortality, but attenuated the associations of vegetables and beans with mortality risk. In conclusion, intakes of plant-based foods, particularly fruit intake, were associated with reduced mortality from CVD and all causes among Japanese men and women.

In 2001, a circular addressing both the composition of school meals and food safety issues was introduced in France to improve the nutrient composition of school meals and provided food-frequency guidelines to guarantee dietary balanced meals. The present study assesses the extent to which secondary state schools are familiar with and implement this circular. In 2005, a nationally representative sample of 1440 secondary state schools received a questionnaire on their catering service and the implementation of the circular's recommendations, and were requested to enclose all menus (lunches and dinners) served over 1 month. Menu analysis shows that progress is still required to achieve a meal composition in accordance with the food-group frequency guidelines appended to the circular. Some recommendations are followed by most of the schools, such as limiting high-fat products and providing plenty of raw fruits and vegetables, cooked vegetables and starchy foods. Other guidelines should be implemented further, especially with regard to the nutritional quality of main courses and dairy products, which are met by less than a third and a half of schools, respectively. Specific efforts are necessary for evening meals to ensure that the nutritional requirements of boarders are covered. Some recommendations, such as the food purchasing manager being trained in nutrition (38 % of schools) and the involvement of dietetic expertise when designing meals (6 %), seem to be linked to better dietary balance of meals. Implementation of the circular must therefore be promoted in schools and may require stronger regulatory nutrition standards and better cooperation between schools.

Dietary energy density (ED) may be a good predictor of weight gain because of its association with the regulation of appetite control signals. Among the participants of the ‘SUpplementation en VItamines et Mineraux AntioXydants’ prospective study, 2707 subjects were included in the present study. Changes in weight, waist circumference (WC), hip circumference (HC) and waist:hip ratio were calculated using measured data collected in 1995/1996 and 2001/2002. The mean changes in various anthropometric indicators according to baseline body-weight status (BMI <  or ≥ 25 kg/m2) and sex-specific tertiles of baseline ED level or 6-year changes in ED were compared by covariance analysis. In overweight subjects, weight gain was positively associated with high dietary ED at baseline (P for trend  =  0·03) and with increasing ED during the follow-up (P for trend  =  0·0008). Both the WC and HC changes were also positively related to baseline ED and change in ED in overweight subjects. However, the relationships observed for the WC and HC changes were no longer significant after adjustment for weight change. These results support the hypothesis of a deleterious effect of high-energy-dense diets on weight change for overweight subjects. This relationship could be mediated by physical activity level. Further research needs to be performed in other populations to determine whether ED could be effective strategies to prevent weight gain.