Lutein, a fat-soluble carotenoid with antioxidant properties, may have an effect on respiratory health. However, the evidence is inconsistent. We aimed to cross-sectionally investigate the association between lutein intake and lung function by measuring forced expiratory volume in 1 s (FEV1), forced vital capacity (FVC) and FEV1/FVC% in adults (aged 45–79 years). We included 4402 participants from the Rotterdam Study, a prospective cohort study in The Netherlands. Lutein intake was assessed using a validated FFQ. Lung function was assessed using spirometry around the same time point as the dietary assessment. No independent association was found between lutein intake and FEV1 (−12·17 (95 % CI −34·21, 9·87) ml per sd increase in lutein) after adjustment for age, sex, height, cohort effect, ethnicity, education, weight, total daily energy intake, smoking status, physical activity, and intakes of fatty acids, dietary fibre, alcohol, β-carotene, β-crypotoxanthin, lycopene and zeaxanthin. There was also no association between lutein and FVC or FEV1/FVC%. However, after stratification by smoking status, lutein intake was significantly associated with lower FEV1/FVC% in current smokers (−1·69 (95 % CI −2·93, −0·45) % per sd increase of lutein) independent of other carotenoids. The present study does not support an independent association between lutein intake and lung function in adults. However, future studies should focus on the potential inverse association between high lutein intake and lung function in specific risk groups such as smokers.

The efficiency with which β-carotene protects against oxidative stress in chicken embryo fibrobiasts (CEF) at low O2 partial pressures was assessed. Primary cultures of CEF were grown at low O2 partial pressures and oxidatively stressed by exposure to paraquat (PQ). Activities of the antioxidant enzymes superoxide dismutase (EC 1.15.1.1; SOD), catalase (EC 1.11.1.6; CAT) and glutathione peroxidase (EC 1.11.1.9; GSH-Px) were measured as indices of oxidative stress. CEF incubated with 0·25–1·0 mM—PQ for 18 h exhibited increased SOD and CAT activities compared with non-PQ-treated control cells (P < 0·001). No cytotoxicity as indicated by lactate dehydrogenase (EC 1.1.1.27; LDH) release was observed at PQ concentrations below 2·0 mM. Incorporation of added β-carotene into 0·25 mM-PQ-treated cells prevented the PQ-induced increases in SOD and CAT, and activities were similar to those seen in non-PQ-treated control cells. GSH-Px activity decreased relative to its control value on exposure to 0·25 mM-PQ and β-carotene prevented this decrease in a dose-dependent manner. The proportion of LDH released from the CEF treated with β-carotene remained below the control value of 2·5% at all times.

We have investigated the effects of maternal diets low in fat or protein, or restricted in total food intake on vitamin A transfer from the dam to her pups. When animals were fed on diets moderately restricted in fat or protein, minimal differences in milk, serum, and liver vitamin A concentrations were observed compared with animals fed on a control diet. In a second study, dams were fed on diets more severely restricted in protein, or fat, or both, or were fed on a control diet equal to 50% of the intake of control rats but containing an equal amount of vitamin A. The quantity of milk obtained from these more severely restricted dams' nipples or the pups' stomachs was greatly reduced; however, there were no differences in milk vitamin A concentration. Body-weight, liver weight, and total liver vitamin A stores of undernourished pups were just half those measured for control pups, although serum vitamin A and serum retinol-binding protein were nearly normal in concentration. We conclude that (a) moderate restrictions in fat or protein in the maternal diet are insufficient to affect transfer of vitamin A to the suckling pup; (b) further dietary restrictions could cause decreased milk production with little change in milk vitamin A concentration and, hence, (c) the neonates' hepatic retinol accumulation during the suckling period is markedly reduced when maternal diets are severely deficient in fat or protein or of normal composition but restricted in amount.

Circulating fetuin-A, a novel marker for hepatic fat accumulation, has been related to a higher risk of type 2 diabetes and cardiovascular diseases in a growing number of prospective studies. However, little is known about dietary determinants of fetuin-A concentrations in the general population. Therefore, we aimed to investigate the association between dietary intake of energy, energy-providing nutrients, alcohol and major food groups and plasma fetuin-A concentrations in the Bavarian Food Consumption Survey II. Dietary intake was assessed by three 24-h dietary recalls, and plasma concentrations of fetuin-A were measured in 558 adults (18–81 years). After multivariable adjustment for lifestyle factors and body fatness, higher energy intake was nonsignificantly associated with higher fetuin-A concentrations (per 2092 kJ/d (500 kcal/d) 3·7 µg/ml, 95 % CI –0·5, 7·8 µg/ml). There was no clear association between energy-providing nutrients and fetuin-A concentrations. Higher alcohol intake was associated with lower fetuin-A concentrations (Ptrend 0·003): mean fetuin-A concentrations were 324 (95 % CI 313, 335) µg/ml in non-drinkers, and with 293 (95 % CI 281, 306) µg/ml significantly lower in participants who drank ≥30 g alcohol per d. Mean fetuin-A concentrations decreased across quintiles of milk and dairy product intake (lowest quintile 319 (95 % CI 309, 330) µg/ml; highest quintile 304 (95 % CI 293, 314) µg/ml; Ptrend 0·03), and each 150-g increment in milk/dairy products per d was associated with 5·6 (95 % CI –9·6, –1·5) µg/ml lower fetuin-A. Dietary intakes of vegetables, meat or fish were not associated with fetuin-A concentrations. Because of the preventive potential of our findings, further exploration is warranted.

Soya foods are one of the recommended alternatives to meat in many dietary guidelines. While this is expected to increase the intake of some nutrients, potential concerns regarding others have been raised. The purpose of the present study was to examine the prevalence and the association of soya food consumption with nutrient intakes and dietary patterns of Canadians (age ≥ 2 years). Cross-sectional data from the 2004 Canadian Community Health Survey (Cycle 2.2; n 33 218) were used to classify soya consumers and non-consumers. Soya consumers were further divided into two groups based on their soya protein intake. Sample weights were applied and logistic regression analysis was used to explore the association between nutrient intakes and soya consumption, with cultural background, sex, age and economic status being included as covariates. On any given day, 3·3 % (n 1085) of Canadians consume soya foods, with females, Asian Canadians and adults with post-secondary education being more likely to be soya consumers. As a whole, adolescent and adult respondents who had consumed at least one soya food during their 24 h dietary recall had higher energy intakes, as well as increased intakes of nutrients such as protein, fibre, vitamin C, vitamin B6, naturally occurring folate, thiamin, Ca, P, Mg, PUFA, Fe and K and lowered intakes of saturated fat. These data indicate that soya food consumption is associated with improved diet quality of Canadians. However, future research is necessary to investigate the association between increased energy intake and soya consumption.

1. The nutrient content and distribution of the carcass meat in broilers (B) and free range cockerels (FR) was studied in two experiments in 1961–2. Half the birds of each type were roasted at 177°C, without additional fat, before dissection and analysis. The breast muscles and red meat were separately analysed for moisture, protein, fat and thiamine. 2. Chunky hybrids (frozen) and Light Sussex × Rhode Island Red (LS × RIR) cockerels were used in both experiments. Expt 1 (group 1) was a pilot study (using groups of six) inwhich B and FR of similar dressed weight were compared. Expt 2 (group 2) consisted of twelve ‘fresh’ (B1) and twelve frozen (B2) broiler hybrids from the same batch of birds killed at 9 weeks; twelve slightly heavier LS × RIR cockerels (FR2) were killed at 18 weeks and twelve Sykes hybrid 3 cockerels (FR1) killed at 20 weeks. The birds received various standard feeds. 3. The edible portion (skin plus meat), expressed as a percentage of the dressed weight, was greater in the free range birds than in the broiler chickens. Increased cooking losses resulting from freezing were responsible for a significantly smaller proportion of edible meat in the cooked frozen broilers. In both groups the edible portion increased with age irrespective of breed or weight. 4. In broiler and free range chickens differenccs in the mean protein content of the total edible meat were small. 5. Fat content appeared to be related to breed as well as to type of bird. In group 1, B contained slightly more fat than FR1. In group 2, B1, and B2, contained significantly more fat then FR1, but the fat content of the raw meat in FR2, was greater. 6. In both experiments the flesh of the free range chickens contained more thiamine than the broiler meat. In group 1 this difference was significant in all the cooked birds; in group 2 significant differences between free range chickens and broilers were found in the breast and red meat of the cooked birds for all comparisons except FR2 and B1. About one-third of the thiamine was lost on cooking both types of chicken in group 1; in group 2 the loss from the broilers was similar but in the FR birds between 18% (FR1) and 26% (FR2) of the thiamine was destroyed. 7. In general the meat of the broilers contained less thiamine and more fat than did that of the free range chickens. Though such differences are of no significance in a mixed diet (as chicken supplies so little thiamine) they are a useful index of differences in nutritive value which result from the different systems of management.

The aim of the present study was to evaluate the impact of infant breast-feeding on cardiovascular risk in young adults. This unique study group involved 158 subjects (eighty-two females) originally collected prospectively at birth in 1975 and followed up to the age of 32 years. Frequent visits during the first year guaranteed the knowledge of the precise duration of breast-feeding. All infants received at least some breast milk. Participants were assessed for both individual cardiovascular risk factors (blood pressure, plasma lipids, homeostatic model assessment of insulin resistance and waist circumference) and the general clinical risk of cardiovascular events by calculating the Framingham risk score (FRS) and the metabolic syndrome criteria score (NCEP-ATPIII; National Cholesterol Education Program's Adult Treatment Panel III). Data on lifestyle factors were carefully collected. Linear regression analyses revealed that the effect of the duration of breast-feeding was not relevant (0·02 decrease in the FRS per one additional breast-feeding month; 95 % CI − 0·19, 0·09). Similarly, the effect of breast-feeding was minor on all of the individual cardiovascular risk factors. We used sex, physical activity, dietary fat and vitamin C, smoking and alcohol consumption as covariates. Again, logistic regression analyses detected no significant impact of the duration of breast-feeding on the risk of the metabolic syndrome according to the NCEP-ATPIII (OR 0·95, 95 % CI 0·8, 1·1). The strongest independent predictor for later CVD risk was male sex. In conclusion, in this prospectively followed cohort of young adults born at term and at weight appropriate for gestational age, the duration of breast-feeding did not have an impact on the accumulation of cardiovascular risk factors.

1. The effects of dietary polychlorinated biphenyls (PCB) and excess tyrosine on serum and liver lipids, urinary ascorbic acid and catecholamines were compared in male Wistar rats.

2. Serum levels of cholesterol, urinary ascorbic acid, norepinephrine, epinephrine, dopamine and histamine were significantly increased in rats given either PCB or excess tyrosine.

3. The hypercholesterolaemia induced by PCB or excess tyrosine was blocked by the adrenergic α-blocker, phenoxybenzamine.

4. The present results suggest causal interrelations between the hypercholesterolaemia induced by dietary PCB or excess tyrosine and the secretion of catecholamines.

The present study explored the hypothesis that a prolonged 8 weeks exposure to a high fructose intake suppresses adrenergic and angiotensin II (Ang II)-mediated vasoconstriction and is associated with a higher contribution of α1D-adrenoceptors. A total of thirty-two Sprague–Dawley rats received either 20 % fructose solution (FFR) or tap water (control, C) to drink ad libitum for 8 weeks. Metabolic and haemodynamic parameters were assessed weekly. The renal cortical vasoconstrictor responses to noradrenaline (NA), phenylephrine (PE), methoxamine (ME) and Ang II were determined in the presence and absence of BMY7378 (α1D-adrenoceptor antagonist). FFR had increased blood pressure, plasma levels of glucose, TAG and insulin. FFR expressed reduced renal vascular responses to adrenergic agonists and Ang II (NA: 50 %, PE: 50 %, ME, 65 %, Ang II: 54 %). Furthermore in the C group, the magnitude of the renal cortical vasoconstriction to all agonists was blunted in the presence of the low or high dose of BMY7378 (NA: 30 and 31 %, PE: 23 and 33 %, ME: 19 and 44 %, Ang II: 53 and 77 %), respectively, while in the FFR, vasoconstriction was enhanced to adrenergic agonists and reduced to Ang II (NA: 8 and 83 %, PE: 55 %, ME, 2 and 177 %, Ang II: 61 and 31 %). Chronic high fructose intake blunts vascular sensitivity to adrenergic agonists and Ang II. Moreover, blocking of the α1D-adrenoceptor subtype results in enhancement of renal vasoconstriction to adrenergic agonists, suggesting an inhibitory action of α1D-adrenoceptors in the FFR. α1D-Adrenoceptors buffer the AT1-receptor response in the renal vasculature of normal rats and fructose feeding suppressed this interaction.

An increased intestinal permeability is associated with several diseases. Previously, we have shown that dietary Ca decreases colonic permeability in rats. This might be explained by a calcium-phosphate-induced increase in luminal buffering capacity, which protects against an acidic pH due to microbial fermentation. Therefore, we investigated whether dietary phosphate is a co-player in the effect of Ca on permeability. Rats were fed a humanised low-Ca diet, or a similar diet supplemented with Ca and containing either high, medium or low phosphate concentrations. Chromium-EDTA was added as an inert dietary intestinal permeability marker. After dietary adaptation, short-chain fructo-oligosaccharides (scFOS) were added to all diets to stimulate fermentation, acidify the colonic contents and induce an increase in permeability. Dietary Ca prevented the scFOS-induced increase in intestinal permeability in rats fed medium- and high-phosphate diets but not in those fed the low-phosphate diet. This was associated with higher faecal water cytotoxicity and higher caecal lactate levels in the latter group. Moreover, food intake and body weight during scFOS supplementation were adversely affected by the low-phosphate diet. Importantly, luminal buffering capacity was higher in rats fed the medium- and high-phosphate diets compared with those fed the low-phosphate diet. The protective effect of dietary Ca on intestinal permeability is impaired if dietary phosphate is low. This is associated with a calcium phosphate-induced increase in luminal buffering capacity. Dragging phosphate into the colon and thereby increasing the colonic phosphate concentration is at least part of the mechanism behind the protective effect of Ca on intestinal permeability.

I deficiency can lead to detrimental effects, particularly in neonates and young infants. The aim of this study was to explore whether postpartum maternal urinary I can be used to estimate the I status of newborns. In this cross-sectional study conducted in Tehran, lactating mothers and newborns, within 3–5 d postpartum, were randomly selected. Urine samples were collected from each mother and newborn, and a heel-prick blood sample was obtained from all newborns as part of the routine national newborn screening programme. According to the WHO criteria, median urinary I concentration (UIC) <100 µg/l and frequency over 3 % of thyroid stimulating hormone (TSH) >5 mIU/l was considered as I insufficiency. A total of 147 postpartum women and neonates, aged 27·8 (sd 5·3) years and 4·2 (sd 0·6) d, respectively, completed this study. The median UIC was 68·0 (interquartile range (IQR) 39·4–133·5) and 212·5 (IQR 92·3–307·3) µg/l in postpartum mothers and newborns, respectively. The median neonatal TSH was 1·00 (IQR 0·50–1·70) mIU/l. There was no significant difference in the neonatal UIC and TSH of infants whose mothers had deficient and sufficient urinary I. In the multiple linear regression, neonatal UIC value was associated with maternal urinary I (P=0·048) and parity (P=0·039); a significant association was observed between neonatal TSH and infant sex (P=0·038) and birth weight (P=0·049). The findings of our study demonstrate that, despite postpartum mothers being mildly I deficient, I status of their infants was adequate as assessed by UIC and TSH values. It seems factors other than maternal urinary I may influence the I status in newborns.

We examined whether there are sex differences in children’s fruit and vegetable (FV) intake and in descriptive norms (i.e. perceived FV intake) related to parents and friends. We also studied whether friends’ impact is as important as that of parents on children’s FV intake. Data from the PRO GREENS project in Finland were obtained from 424 children at the age 11 years at baseline. At baseline, 2009 children filled in a questionnaire about descriptive norms conceptualised as perceived FV intake of their parents and friends. They also filled in a validated FFQ that assessed their FV intake both at baseline and in the follow-up in 2010. The associations were examined with multi-level regression analyses with multi-group comparisons. Girls reported higher perceived FV intake of friends and higher own fruit intake at baseline, compared with boys, and higher vegetable intake both at baseline and in the follow-up. Perceived FV intake of parents and friends was positively associated with both girls’ and boys’ FV intake in both study years. The impact of perceived fruit intake of the mother was stronger among boys. The change in children’s FV intake was affected only by perceived FV intake of father and friends. No large sex differences in descriptive norms were found, but the impact of friends on children’s FV intake can generally be considered as important as that of parents. Future interventions could benefit from taking into account friends’ impact as role models on children’s FV intake.

1. Deficiency of zinc inhibits growth and also increases the activity of alkaline ribonuclease in certain tissues of the rat (Prasad & Oberleas, 1973). Zn could influence ribonuclease activity by direct effects on the enzyme or its natural inhibitor, or non-specifically as occurs when growth rate is affected by various other factors. These possibilities were studied.

2. Alkaline ribonuclease was shown to be inhibited by Zn in vitro, but the concentrations of Zn required were so high that the enzyme was probably not directly affected by changes in tissue Zn concentration caused by dietary deficiency.

3. At lower concentrations, Zn added in vitro increased the activity of alkaline ribonuclease in tissue homogenates probably by inactivating the inhibitor of the enzyme.

4. Age, weight and particularly food restriction caused tissue-specific alterations of ribonuclease and ribonuclease inhibitor concentrations in liver, kidney, oesophagus, testis and thymus.

5. The ribonuclease activities in liver, kidney and testis of Zn-deficient rats were unaltered in comparison with those of pair-fed rats. In thymus, which decreased in weight in the Zn-deficient animals, there was a concomitant increase in ribonuclease activity, but in oesophagus, the deficiency reduced the activity of ribonuclease.

6. The effects of Zn deficiency upon alkaline ribonuclease and its inhibitor are probably secondary consequences of reductions in food intake or growth.

American mink (Neovison vison) develop fatty liver quickly in response to food deprivation, which results in preferential mobilisation of n-3 PUFA. The altered n-3:n-6 PUFA ratio in the liver may activate the endocannabinoid system resulting in increased lipid synthesis. The objective of the present study was to investigate the effects of feeding intensity (80 or 120 % RDA), dietary fat source (n-3, n-6 or n-9 fatty acids (FA)) and short-term fasting (1–7 d) on hepatic de novo lipogenesis (DNL) and the development of fatty liver in mink. Significantly elevated expression of mRNA encoding for acetyl-CoA carboxylase-1 (ACC-1) and FA synthase (FAS) was observed in the liver of mink fasted for 5–7 d, while upon re-feeding for 28 d after a 7 d food deprivation, DNL returned to pre-fasting levels. The females had a higher expression of ACC-1 and FAS mRNA than the males. In the non-fasted animals, dietary fat source and feeding intensity had significant effects on ACC-1 mRNA. The highest levels were observed in the mink fed the rapeseed oil (n-9) diet at 80 % RDA, while the lowest levels were seen when the same diet was fed at 120 % RDA. For FAS, the highest gene expression was seen in the fasted mink fed at 80 % RDA and the lowest in the non-fasted mink fed at 80 %. It is concluded that short-term food deprivation induces hepatic lipidosis in mink and that during this process, hepatic DNL further exacerbates liver fat accumulation.