Soya proteins and isoflavones have been reported to exert beneficial effects on the serum lipid profile. More recently, this claim is being challenged. The objective of this study was to comprehensively examine the effects of soya consumption on the lipid profile using published trials. A detailed literature search was conducted via MEDLINE (from 2004 through February 2014), CENTRAL (The Cochrane Controlled Clinical Trials Register) and ClinicalTrials.gov for randomised controlled trials assessing the effects of soya on the lipid profile. The primary effect measure was the difference in means of the final measurements between the intervention and control groups. In all, thirty-five studies (fifty comparisons) were included in our analyses. Treatment duration ranged from 4 weeks to 1 year. Intake of soya products resulted in a significant reduction in serum LDL-cholesterol concentration, –4·83 (95 % CI –7·34, –2·31) mg/dl, TAG, –4·92 (95 % CI –7·79, –2·04) mg/dl, and total cholesterol (TC) concentrations, –5·33 (95 % CI –8·35, –2·30) mg/dl. There was also a significant increase in serum HDL-cholesterol concentration, 1·40 (95 % CI 0·58, 2·23) mg/dl. The I2 statistic ranged from 92 to 99 %, indicating significant heterogeneity. LDL reductions were more marked in hypercholesterolaemic patients, –7·47 (95 % CI –11·79, –3·16) mg/dl, than in healthy subjects, –2·96 (95 % CI –5·28, –0·65) mg/dl. LDL reduction was stronger when whole soya products (soya milk, soyabeans and nuts) were used as the test regimen, –11·06 (95 % CI –15·74, –6·37) mg/dl, as opposed to when ‘processed’ soya extracts, –3·17 (95 % CI –5·75, –0·58) mg/dl, were used. These data are consistent with the beneficial effects of soya proteins on serum LDL, HDL, TAG and TC concentrations. The effect was stronger in hypercholesterolaemic subjects. Whole soya foods appeared to be more beneficial than soya supplementation, whereas isoflavone supplementation had no effects on the lipid profile.

Folate is an essential B vitamin required for de novo purine and thymidylate synthesis, and for the remethylation of homocysteine to form methionine. Folate deficiency has been associated with placenta-related pregnancy complications, as have SNP in genes of the folate-dependent enzymes, methionine synthase (MTR) and methylenetetrahydrofolate dehydrogenase 1 (MTHFD1). We aimed to determine the effect of altered folate metabolism on placental cell proliferation, viability and invasive capacity and on progesterone and human chorionic gonadotropin (hCG) secretion. Human placental choriocarcinoma (JEG-3) cells cultured in low folic acid (FA) (2 nm) demonstrated 13 % (P<0·001) and 26 % (P<0·001) lower proliferation, 5·5 % (P=0·025) and 7·5 % (P=0·004) lower invasion capacity, and 5 to 7·5 % (P=0·004–0·025) lower viability compared with control (20 nm) or supplemented (100 nm) cells, respectively. FA concentration had no effect on progesterone or hCG secretion. Small interfering RNA (siRNA) knockdown of MTR gene and protein expression resulted in 17·7 % (P<0·0001) lower proliferation and 61 % (P=0·014) higher progesterone secretion, but had no effect on cell invasion and hCG secretion. siRNA knockdown of MTHFD1 gene expression in the absence of detectable changes in protein expression resulted in 10·3 % (P=0·001) lower cell proliferation, but had no effect on cell invasion and progesterone or hCG secretion. Our data indicate that impaired folate metabolism can result in lower trophoblast proliferation, and could alter viability, invasion capacity and progesterone secretion, which may explain in part the observed associations between folate and placenta-related complications.

Polyphenols have been described to have a wide range of biological activities, and many reports, published during recent years, have highlighted the beneficial effects of phenolic compounds, illustrating their promising role as therapeutic tools in several acute and chronic disorders. The purpose of study was to evaluate, in an already-assessed model of lung injury caused by bleomycin (BLM) administration, the role of resveratrol and quercetin, as well as to explore the potential beneficial properties of a mango leaf extract, rich in mangiferin, and a grape leaf extract, rich in dihydroquercetin (DHQ), on the same model. Mice were subjected to intra-tracheal administration of BLM, and polyphenols were administered by oral route immediately after BLM instillation and daily for 7 d. Treatment with resveratrol, mangiferin, quercetin and DHQ inhibited oedema formation and body weight loss, as well as ameliorated polymorphonuclear infiltration into the lung tissue and reduced the number of inflammatory cells in bronchoalveolar lavage fluid. Moreover, polyphenols suppressed inducible nitric oxide synthase expression, and prevented oxidative and nitroxidative lung injury, as shown by the reduced nitrotyrosine and poly (ADP-ribose) polymerase levels. The degree of apoptosis, as evaluated by Bid and Bcl-2 balance, was also suppressed after polyphenol treatment. Finally, these natural products down-regulated cyclo-oxygenase-2, extracellular signal-regulated kinase phosphorylated expression and reduced NF-κBp65 translocation. Our findings confirmed the anti-inflammatory effects of resveratrol and quercetin in BLM-induced lung damage, and highlight, for the first time, the protective properties of exogenous administration of mangiferin and DHQ on experimental pulmonary fibrosis.

n-3 Long-chain PUFA up-regulate intestinal lipid metabolism. However, whether these metabolic effects of PUFA on intestine are mediated by AMP-activated protein kinase (AMPK) remains to be elucidated. To determine the effects of α-linolenic acid (ALA) on intestinal fatty acid (FA) metabolism and whether these effects were affected by AMPK deletion, mice deficient in the catalytic subunit of AMPKα1 or AMPKα2 and wild-type (WT) mice were fed either a high-fat diet (HF) or HF supplemented with ALA (HF-A). The results showed that ALA supplementation decreased serum TAG content in WT mice. ALA also increased mRNA expression of genes (carnitine palmitoyltransferase 1a, acyl-CoA oxidase 1, medium-chain acyl-CoA dehydrogenase, cytochrome P450 4A10 and pyruvate dehydrogenase kinase isoenzyme 4a) involved in intestinal lipid oxidation and mRNA expression of TAG synthesis-related genes (monoacylglycerol O-acyltransferase 2, diacylglycerol O-acyltransferases 1 and 2) in WT mice. Consistent with these, expression levels of phosphorylated AMPKα1 and AMPKα2 were also increased in WT mice after ALA addition. However, in the absence of either AMPKα1 or AMPKα2, ALA supplementation failed to increase intestinal lipid oxidation. In addition, no significant effects of either diet (HF and HF-A) or genotype (WT, AMPKα1–/– and AMPKα2–/–) on FA uptake in the intestine and faecal TAG output were observed. Our results suggest that AMPK is indispensable for the effects of ALA on intestinal lipid oxidation.

Dietary fish oil (FO) modulates muscle O2 consumption and contractile function, predictive of effects on muscle fatigue. High doses unattainable through human diet and muscle stimulation parameters used engender uncertainty in their physiological relevance. We tested the hypothesis that nutritionally relevant FO doses can modulate membrane fatty acid composition and muscle fatigue. Male Sprague–Dawley rats were randomised to control (10 % olive oil (OO) by weight) or low or moderate FO diet (LowFO and ModFO) (HiDHA tuna fish oil) for 15 weeks (LowFO: 0·3 % FO, 9·7 % OO, 0·25 % energy as EPA+DHA; ModFO: 1·25 % FO, 8·75 % OO, 1·0 % energy as EPA+DHA). Hindlimb muscle function was assessed under anaesthesia in vivo using repetitive 5 s burst sciatic nerve stimulation (0·05 ms, 7–12 V, 5 Hz, 10 s duty cycle, 300 s). There were no dietary differences in maximum developed muscle force. Repetitive peak developed force fell to 50 % within 62 (sem 10) s in controls and took longer to decline in FO-fed rats (LowFO 110 (sem 15) s; ModFO 117 (sem 14) s) (P<0·05). Force within bursts was better sustained with FO and maximum rates of force development and relaxation declined more slowly. The FO-fed rats incorporated higher muscle phospholipid DHA-relative percentages than controls (P<0·001). Incorporation of DHA was greater in the fast-twitch gastrocnemius (Control 9·3 (sem 0·8) %, LowFO 19·9 (sem 0·4), ModFO 24·3 (sem 1·0)) than in the slow-twitch soleus muscle (Control 5·1 (sem 0·2), LowFO 14·3 (sem 0·7), ModFO 18·0 (sem 1·4)) (P<0·001), which was comparable with the myocardium, in line with muscle fibre characteristics. The LowFO and ModFO diets, emulating human dietary and therapeutic supplement intake, respectively, both elicited muscle membrane DHA enrichment and fatigue resistance, providing a foundation for translating these physiological effects to humans.

A randomised controlled trial (RCT) of high-dose v. low-dose fish oil in recent-onset rheumatoid arthritis (RA) demonstrated that the group allocated to high-dose fish oil had increased remission and decreased failure of disease-modifying anti-rheumatic drug (DMARD) therapy. This study examines the relationships between plasma phospholipid levels of the n-3 fatty acids in fish oil, EPA and DHA, and remission and DMARD use in recent-onset RA. EPA and DHA were measured in blood samples from both groups of the RCT. The data were analysed as a single cohort, and Cox proportional hazards models were used to examine relationships between plasma phospholipid (PL) EPA and DHA and various outcome measures. When analysed as a single cohort, plasma PL EPA was related to time to remission, with a one unit increase in EPA (1 % total fatty acids) associated with a 12 % increase in the probability of remission at any time during the study period (hazard ratio (HR)=1·12; 95 % CI 1·02, 1·23; P=0·02). Adjustment for smoking, anti-cyclic citrullinated peptide antibodies and ‘shared epitope’ HLA-DR allele status did not change the HR. Plasma PL EPA, adjusted for the same variables, was negatively related to time to DMARD failure (HR=0·85; 95 % CI 0·72, 0·99; P=0·047). The HR for DHA and time to remission or DMARD failure were similar in magnitude to those for EPA, but not statistically significant. Biomarkers of n-3 status, such as plasma PL EPA, have the potential to predict clinical outcomes relevant to standard drug treatment of RA patients.

Breast milk long-chain PUFA (LCPUFA) have been associated with changes in early life immune responses and may modulate T-cell function in infancy. We studied the effect of maternal fatty acid desaturase (FADS) genotype and breast milk LCPUFA levels on infants’ blood T-cell profiles and ex vivo-produced cytokines after anti-CD3/CD28 stimulation of peripheral blood mononuclear cells in 6-month-old infants from the Copenhagen Prospective Study of Asthma in Childhood birth cohort. LCPUFA concentrations of breast milk were assessed at 4 weeks of age, and FADS SNP were determined in both mothers and infants (n 109). In general, breast milk arachidonic acid (AA) levels were inversely correlated with the production of IL-10 (r −0·25; P=0·004), IL-17 (r −0·24; P=0·005), IL-5 (r −0·21; P=0·014) and IL-13 (r −0·17; P=0·047), whereas EPA was positively correlated with the counts of blood regulatory T-cells and cytotoxic T-cells and decreased T-helper cell counts. The minor FADS alleles were associated with lower breast milk AA and EPA, and infants of mothers carrying the minor allele of FADS SNP rs174556 had higher production of IL-10 (r −0·23; P=0·018), IL-17 (r −0·25; P=0·009) and IL-5 (r −0·21; P=0·038) from ex vivo-activated immune cells. We observed no association between T-cell distribution and maternal or infant FADS gene variants. We conclude that increased maternal LCPUFA synthesis and breast milk AA are associated with decreased levels of IL-5, IL-13 (type-2 related), IL-17 (type-17 related) and IL-10 (regulatory immune responses), but not with interferon-γ and TNF-α, which could be due to an effect of the maternal FADS variants on the offspring immune response transferred via breast milk LCPUFA.

Certain purified indigestible carbohydrates such as inulin have been shown to stimulate gut-derived hormones involved in glycaemic regulation and appetite regulation, and to counteract systemic inflammation through a gut microbiota-mediated mechanism. Less is known about the properties of indigestible carbohydrates intrinsic to food. The aim of this study was to investigate the possibility to affect release of endogenous gut hormones and ameliorate appetite control and glycaemic control by ingestion of a whole-grain cereal food product rich in NSP and resistant starch in healthy humans. In all, twenty middle-aged subjects were provided with a barley kernel-based bread (BB) or a reference white wheat bread during 3 consecutive days, respectively, in a randomised cross-over design study. At a standardised breakfast the following day (day 4), blood was collected for the analysis of blood (b) glucose regulation, gastrointestinal hormones, markers of inflammation and markers of colonic fermentation; 3 d of intervention with BB increased gut hormones in plasma (p) the next morning at fasting (p-glucagon-like peptide-1; 56 %) and postprandially (p-glucagon-like peptide-2; 13 % and p-peptide YY; 18 %). Breath H2 excretion and fasting serum (s) SCFA concentrations were increased (363 and 18 %, respectively), and b-glucose (22 %) and s-insulin responses (17 %) were decreased after BB intervention. Insulin sensitivity index (ISIcomposite) was also improved (25 %) after BB. In conclusion, 3 d of intervention with BB increased systemic levels of gut hormones involved in appetite regulation, metabolic control and maintenance of gut barrier function, as well as improved markers of glucose homoeostasis in middle-aged subjects, altogether relevant for the prevention of obesity and the metabolic syndrome.

This study investigated the effect of a caffeinated energy drink on various aspects of performance in sprint swimmers. In a randomised and counterbalanced order, fourteen male sprint swimmers performed two acute experimental trials after the ingestion of a caffeinated energy drink (3 mg/kg) or after the ingestion of the same energy drink without caffeine (0 mg/kg; placebo). After 60 min of ingestion of the beverages, the swimmers performed a countermovement jump, a maximal handgrip test, a 50 m simulated competition and a 45 s swim at maximal intensity in a swim ergometer. A blood sample was withdrawn 1 min after the completion of the ergometer test. In comparison with the placebo drink, the intake of the caffeinated energy drink increased the height in the countermovement jump (49·4 (sd 5·3) v. 50·9 (sd 5·2) cm, respectively; P<0·05) and maximal force during the handgrip test with the right hand (481 (sd 49) v. 498 (sd 43) N; P<0·05). Furthermore, the caffeinated energy drink reduced the time needed to complete the 50 m simulated swimming competition (27·8 (sd 3·4) v. 27·5 (sd 3·2) s; P<0·05), and it increased peak power (273 (sd 55) v. 303 (sd 49) W; P<0·05) and blood lactate concentration (11·0 (sd 2·0) v. 11·7 (sd 2·1) mm; P<0·05) during the ergometer test. The caffeinated energy drink did not modify the prevalence of insomnia (7 v. 7 %), muscle pain (36 v. 36 %) or headache (0 v. 7 %) during the hours following its ingestion (P>0·05). A caffeinated energy drink increased some aspects of swimming performance in competitive sprinters, whereas the side effects derived from the intake of this beverage were marginal at this dosage.

A higher fat content in the diet could be an advantage for preventing malnutrition among older adults. However, there is sparse scientific evidence to determine the optimal fat intake among older adults. This prospective cohort study examined whether a high energy intake of dietary fat among middle-aged and older adults is associated with the risk of malnutrition 10 years later. The study population comprised 725 Swedish men and women aged 53–80 years who had completed a questionnaire about dietary intake and lifestyle factors in 1997 (baseline) and whose nutritional status was assessed when admitted to the hospital in 2008–2009 (follow-up). At the follow-up, 383 (52·8 %) participants were identified as being at risk of malnutrition and fifty-two (7·2 %) were identified as malnourished. Multinomial logistic regression models were used to analyse the association between previous dietary fat intake and nutritional status later in life. Contrary to what was expected, a high energy intake from total fat, saturated fat and monounsaturated fat among middle-aged and older adults increased the risk of exhibiting malnutrition 10 years later. However, this applied only to individuals with a BMI<25 kg/m2 at the baseline. In conclusion, these findings suggest that preventive actions to counteract malnutrition in older adults should focus on limiting the intake of total fat in the diet by reducing consumption of food with a high content of saturated and monounsaturated fat.

Higher dietary intakes of Mg and Ca, individually, have been associated with a decreased risk for the metabolic syndrome (MetSyn). Experimental studies suggest that a higher intra-cellular ratio of Ca:Mg, which may be induced by a diet high in Ca and low in Mg, may lead to hypertension and insulin resistance. However, no previous epidemiological studies have examined the effects of the combined intake of Mg and Ca on MetSyn. Thus, we evaluated the association between dietary intakes of Ca and Mg (using 24-h recalls), independently and in combination, and MetSyn in the National Health and Nutrition Examination Study 2001–2010 data, which included 9148 adults (4549 men and 4599 women), with complete information on relevant nutrient, demographic, anthropometric and biomarker variables. We found an inverse association between the highest (>355 mg/d) v. the lowest (<197 mg/d) quartile of Mg and MetSyn (OR 0·70; 95 % CI 0·57, 0·86). Women who met the RDA for both Mg (310–320 mg/d) and Ca (1000–1200 mg/d) had the greatest reduced odds of MetSyn (OR 0·59; 95 % CI 0·45, 0·76). In men, meeting the RDA for Mg (400–420 mg/d) and Ca (1000–1200 mg/d), individually or in combination, was not associated with MetSyn; however, men with intakes in the highest quartile for Mg (≥386 mg/d) and Ca (≥1224 mg/d) had a lower odds of MetSyn (OR 0·74; 95 % CI 0·59, 0·93). Our results suggest that women who meet the RDA for Mg and Ca have a reduced odds of MetSyn but men may require Ca levels higher than the RDA to be protected against MetSyn.

Decreasing sodium intake has been associated with improvements in blood pressure (BP) and proteinuria, two important risk factors for CVD and chronic kidney disease (CKD) progression. We aimed to investigate the role of sodium intake by examining the effect of changes in sodium intake over 1 year on BP and proteinuria in people with early stage CKD. From thirty-two general practices, 1607 patients with previous estimated glomerular filtration rate of 59–30 ml/min per 1·73 m2 and mean age of 72·9 (sd 9·0) years were recruited. Clinical assessment, urine and serum biochemistry testing were performed at baseline and after 1 year. Sodium intake was estimated from early morning urine specimens using an equation validated for this study population. We found that compared with people who increased their sodium intake from ≤100 to >100 mmol/d over 1 year, people who decreased their intake from >100 to ≤100 mmol/d evidenced a greater decrease in all BP variables (Δmean arterial pressure (ΔMAP)=–7·44 (sd 10·1) v. –0·23 (sd 10·4) mmHg; P<0·001) as well as in pulse wave velocity (ΔPWV=–0·47 (sd 1·3) v. 0·08 (sd 1·88) m/s; P<0·05). Albuminuria improved only in albuminuric patients who decreased their sodium intake. BP improved in people who maintained low sodium intake at both times and in those with persistent high intake, but the number of anti-hypertensive increased only in the higher sodium intake group, and PWV improved only in participants with lower sodium intake. Decreasing sodium intake was an independent determinant of ΔMAP. Although more evidence is needed, our results support the benefits of reducing and maintaining sodium intake below 100 mmol/d (2·3–2·4 g/d) in people with early stages of CKD.

Little is known about the clustering patterns of lifestyle behaviours in adult populations. We explored clusters in multiple lifestyle behaviours including physical activity (PA), smoking, alcohol use and eating habits in a sample of adult population. A cross-sectional and multi-centre study was performed with six participating groups distributed throughout Spain. Participants (n 1327) were part of the Lifestyles and Endothelial Dysfunction (EVIDENT) study and were aged between 20 and 80 years. The lifestyle and cardiovascular risk (CVR) factors were analysed using a clustering method based on the HJ-biplot coordinates to understand the variables underlying these groupings. The following three clusters were identified. Cluster 1: unhealthy, 677 subjects (51 %), with a slight majority of men (58·7 %), who were more sedentary and smokers with higher consumption of whole-fat dairy products, bigger waist circumference as well as higher TAG levels, systolic blood pressure (SBP) and CVR. Cluster 2: healthy/PA, 265 subjects (20 %), including 24·0 % of males with high PA. Cluster 3: healthy/diet, including 29 % of the participants, with a higher consumption of olive oil, fish, fruits, nuts, vegetables and lower alcohol consumption. Using the unhealthy cluster as a reference, and after adjusting for age and sex, the multiple regression analysis showed that belonging to the healthy/PA cluster was associated with a lower waist circumference, body fat percentage, SBP and CVR. In summary, the three clusters were identified according to lifestyles. The ‘unhealthy’ cluster had the least favourable clinical parameters, the ‘healthy/PA’ cluster had good HDL-cholesterol levels and low SBP and the ‘healthy/diet’ cluster had lower LDL-cholesterol levels and clinical blood pressure.

It has been shown that food insecurity is associated with poor diet quality and unfavourable health outcomes. However, little is known about the potential effects of food insecurity on the overall malnutrition status among children. In this study, we investigated the prevalence of food insecurity among 1583 elementary school students, aged 6–14 years, living in Chinese rural areas and examined its association with four malnutrition signs, including rickets sequelae, anaemia, stunting and wasting. Information on food security was collected via questionnaires. Rickets sequelae were assessed by an experienced paediatrician during the interview. Anaemia was determined by the WHO Hb thresholds adjusted by the local altitude. Weight and height were measured during the interview. Stunting and wasting were then evaluated according to WHO child growth standards (2007). We examined the association between food insecurity and the number of malnutrition signs (total number=4), and the likelihood of having severe malnutrition (presence of 3+ signs), after adjusting for potential confounders, such as age, social-economic status and dietary intakes. During the previous 12 months, the overall prevalence of food insecurity was 6·1 % in the entire studied population and 16·3 % in participants with severe malnutrition. Participants with food insecurity had a slightly higher number of malnutrition signs (1·14 v. 0·96; P=0·043) relative to those who were food secure, after adjusting for potential confounders. Food insecurity was also associated with increased likelihood of having severe malnutrition (adjusted OR 3·08; 95 % CI 1·47, 6·46; P=0·003). In conclusion, food insecurity is significantly associated with malnutrition among Chinese children in this community.

Studies on fibre intake and incident colorectal cancer (CRC) indicate inverse associations. Differences by tumour stage have not been examined. We examined associations between fibre intake and its sources, and incidental CRC. Separate analyses were carried out on the basis of sex, tumour location and the Tumour, Node, Metastasis (TNM) classification. The Malmö Diet and Cancer Study is a population-based cohort study, including individuals aged 45–74 years. Dietary data were collected through a modified diet history method. The TNM classification was obtained from pathology/clinical records and re-evaluated. Among 27 931 individuals (60 % women), we found 728 incident CRC cases during 428 924 person-years of follow-up. Fibre intake was inversely associated with CRC risk (Ptrend=0·026). Concerning colon cancer, we observed borderline interaction between fibre intake and sex (P=0·052) and significant protective association restricted to women (Ptrend=0·013). Intake of fruits and berries was inversely associated with colon cancer in women (Ptrend=0·022). We also observed significant interactions between intakes of fibre (P=0·048) and vegetables (P=0·039) and sex on rectal cancer, but no significant associations were seen between intake of fibre, or its sources, in either of the sexes. Except for inverse associations between intake of fibre-rich cereal products and N0- and M0-tumours, we did not observe significant associations with different TNM stages. Our findings suggest different associations between fibre intake and CRC depending on sex, tumour site and fibre source. High fibre intake, especially from fruits and berries, may, above all, prevent tumour development in the colon in women. No clear differences by TNM classification were detected.

Lutein is a carotenoid with strong antioxidant properties. Previous studies in adults suggest a beneficial role of lutein on cardiometabolic health. However, it is unknown whether this relation also exists in children; therefore, we aimed to assess the relation between lutein intake at 13 months of age and cardiometabolic outcomes at the age of 6 years. We included 2044 Dutch children participating in a population-based prospective cohort study. Diet was measured at 13 months of age with an FFQ. Lutein intake was standardised for energy and β-carotene intake. Blood pressure, anthropometrics, serum lipids and insulin were measured at the age of 6 years. Dual-energy X-ray absorptiometry was performed to measure total and regional fat and lean mass. A continuous cardiometabolic risk factor score was created, including the components body fat percentage, blood pressure, insulin, HDL-cholesterol and TAG. Age- and sex-specific standard deviation scores were created for all outcomes. Multivariable linear regression was performed, including socio-demographic and lifestyle variables. Median (energy-standardised) lutein intake was 1317 mcg/d (95 % range 87, 6069 mcg/d). There were no consistent associations between lutein intake at 13 months and anthropometrics and body composition measures at 6 years of age. In addition, lutein intake was not associated with a continuous cardiometabolic risk factor score, nor was it associated with any of the individual components of the cardiometabolic risk factor score. Results from this large population-based prospective cohort study do not support the hypothesis that lutein intake early in life has a beneficial role for later cardiometabolic health.

The aim of this study was to describe the change in vegetable consumption with ageing and the transition to retirement. Study subjects were the participants of the GAZEL prospective cohort (Gaz and Électricité de France) aged 40–49 years at inclusion in 1989 who retired between 1991 and 2008 (12 942 men and 2739 women). Four FFQ were completed from 1990 to 2009. We used multiple imputation by chained equations in order to avoid dropping incomplete cases. The OR for eating vegetables everyday was estimated as a function of ageing, retirement status and the place of lunch before retirement through generalised estimating equations. Analyses were stratified by sex, and models were adjusted for confounders, including current spousal status. In 1990, 17·7 % of men and 31 % of women reported eating vegetables daily. The odds of consuming vegetables everyday increased with ageing for both men and women. The usual place of lunch was home for less than half the sample before retirement and for almost every respondent after retirement. For those who changed their place of lunch, the association between being retired and the odds of eating vegetables daily was positive and significant. We found that, in this cohort, vegetable consumption increased with ageing. Retirement had an indirect effect on vegetable consumption mediated by changes in the place of lunch.

Children’s learning about food is considerable during their formative years, with parental influence being pivotal. Research has focused predominantly on maternal influences, with little known about the relationships between fathers’ and children’s diets. Greater understanding of this relationship is necessary for the design of appropriate interventions. The aim of this study was to investigate the associations between the diets of fathers and their children and the moderating effects of fathers’ BMI, education and age on these associations. The diets of fathers and their first-born children (n 317) in the Melbourne Infant Feeding Activity and Nutrition Trial (InFANT) Program were assessed using an FFQ and 3×24-h recalls, respectively. The InFANT Program is a cluster-randomised controlled trial in the setting of first-time parents groups in Victoria, Australia. Associations between father and child fruit, vegetable, non-core food and non-core drink intakes were assessed using linear regression. The extent to which these associations were mediated by maternal intake was tested. Moderation of associations by paternal BMI, education and age was assessed. Positive associations were found between fathers’ and children’s intake of fruit, sweet snacks and take-away foods. Paternal BMI, education and age moderated the relationships found for the intakes of fruit (BMI), vegetables (age), savoury snacks (BMI and education) and take-away foods (BMI and education). Our findings suggest that associations exist at a young age and are moderated by paternal BMI, education and age. This study highlights the importance of fathers in modelling healthy diets for their children.

In the abstract, these sentences (page 1, line 5) should be: ‘Additionally, hepatic betaine–homocysteine methyltransferase concentration as well as its mRNA abundance and lecithin level were found increased (P<0·05) by betaine supplementation in both basal diet-fed rats and high-fat diet-fed rats. Betaine administration in high-fat diet-fed rats exhibited a higher (P<0·05) concentration of hepatic carnitine palmitoyltransferase 1 (CPT1) comparedwith high-fat diet-fed rats.’