1. The effect of xylitol feeding on the iron content of rat tissues was studied.

2. Adult male rats were fed on the basal diet containing (g/kg) 200 glucose, or 50 or 200 xylitol, or the same diet containing no added carbohydrates for 8 weeks. Each feeding group comprised nine animals.

3. Xylitol at 200 g/kg diet retarded the growth rate of the rats, whereas 200 g glucose/kg increased the weight gains compared with animals given no added carbohydrates.

4. Xylitol at 50 g/kg did not affect the tissue Fe concentrations, but 200 g xylitol/kg increased the Fe content of the livers, duodenum wall, spleen, bone marrow and serum.

5. Cadmium and lead contents of the livers were similar in all groups.

6. Xylitol–Fe complexes are suggested to be responsible for the increased Fe absorption during xylitol feeding.

The relationship between digestive enzyme activities in the pancreas and pancreatic juice was studied in post-weaning rats fed on a low-protein diet (30 g cereal protein/kg) for 1 month and a refeeding balanced diet (235 g mixed protein/kg) for the following 3 months. A control group was fed on the balanced diet for 4 months. At the end of malnutrition and at various times of refeeding, activities of amylase (EC 3.2.1.1), trypsin(EC 3.4.21.4), chymotrypsin (EC 3.4.21.1), lipase (EC 3.1.1.3), phospholipase A2 (EC 3.1.1.4) and cholesterolesterase (EC 3.1.1.13) in pancreas and pancreatic juice were measured. Recovery of body and pancreas weights was obtained after 3 months of refeeding. Pancreas offered a higher resistance to the low-protein diet; a quicker recovery than that of the whole organism was observed during refeeding. Protein and RNA contents of pancreatic cells were depressed by protein depletion. At the end of refeeding, pancreatic and cell RNA contents were still depressed. In pancreas and pancreatic juice, protein depletion produced a decrease in enzyme activities, with the exception of phospholipase A2 and cholesterolesterase. During refeeding, activities were increased to various levels in pancreatic juice and pancreas. In pancreatic juice, a deficit in enzyme activities still prevailed at the end of refeeding. The retention thresholds (total activity in pancreas v. activity per h in pancreatic juice) of hydrolases were increased by malnutrition. They were all decreased by refeeding at various rates, but after 3 months of refeeding the thresholds were still markedly increased for all enzymes studied. After malnutrition and during refeeding, the dissociated enzyme activities in pancreas and pancreatic juice could be the expression of an alteration at different stages: synthesis, intracellular transport, storage mechanisms and secretion.

Fish-oil supplements are marketed as enhancing intelligence and cognitive performance. However, empirical data concerning the utility of these products in healthy term infants are mixed, particularly with respect to lasting effects into childhood. We evaluated whether fish-oil supplementation during infancy leads to better neurocognitive/behavioural development at 6 years. We conducted a double-blind randomised controlled trial of supplementation with n-3 long-chain PUFA in 420 healthy term infants. Infants received either fish oil (containing at least 250 mg DHA and at least 60 mg EPA) or placebo (olive oil) daily from birth to 6 months of age. Neurodevelopmental follow-up was conducted at a mean age of 6 years (sd 7 months), whereby 335 children were assessed for language, executive functioning, global intelligence quotient and behaviour. No significant differences were observed between the groups for the main neurocognitive outcomes. However in parent-report questionnaire, fish-oil supplementation was associated with negative externalising (P = 0·035, d = 0·24) and oppositional/defiant behaviour (P = 0·006, d = 0·31), particularly in boys (P = 0·01, d = 0·45; P = 0·004, d = 0·40). Our results provide evidence that fish-oil supplementation to predominantly breast-fed infants confers no significant cognitive or behavioural benefit to children at 6 years.

To evaluate some of the mechanisms involved in the plasma cholesterol lowering of sitostanol (SI), male Hartley guinea pigs were fed diets containing cholesterol (0.25 g/100 g) and four doses of SI: either 0 (control), 0.75, 1.5 or 2.25 g/100 g. In addition a negative control (-C) group with dietary cholesterol (0.04 g/100 g) was included. Corn oil was used as the source of fat and the contribution of fat energy was 35 %. Plasma total cholesterol was 43, 49 and 53 % (P<0.0001) lower after SI intake compared to the control. Plasma LDL concentrations were 47, 53 and 61 % lower with increasing doses of SI. In addition, intake of SI resulted in 26–42 % lower hepatic total cholesterol. Hepatic esterified cholesterol and triacylglycerols were 32–60 % and 55–61 % lower after SI intake. SI intake resulted in favourable plasma and hepatic cholesterol concentrations similar to those in guinea pigs fed low levels of dietary cholesterol (-C). The LDL obtained from the control group had a higher number of molecules of free and esterified cholesterol than the SI groups. SI intake resulted in 69–71 % higher cholesterol excretion compared to the control. SI treatment enhanced the total faecal neutral sterol excretion by 54–58 % compared to control and by 70–76 % compared to the (-C) group. These results suggest that SI might have its hypocholesterolaemic effect by reducing cholesterol absorption, which results in lower concentration of cholesterol in liver. This reduction in hepatic cholesterol might possibly alter hepatic cholesterol metabolism and affect lipoprotein concentration and composition.

1. Urinary excretions of creatinine (Cre) and hydroxyproline (OHPr) were measured in two groups of children: (a) 24 h collections in male and ‘spot’ samples in female marasmic infants throughout the course of treatment, and (b) ‘spot’ samples in underprivileged pre-school children at home. Results were related to certain somatic measurements and in some instances to some dietary factors.

2. Analysis of 24 h samples taken at intervals throughout 120 d of treatment showed a steady rise towards normal levels from very low initial values of OHPr. There was no corre-lation with age or body-weight on admission, nor of OHPr excretion through recovery with increase in height. Excretion of Cre also increased during recovery but the trend was more erratic. There was no relation to initial weight deficit or age but mean Cre excretion through recovery did correlate with rate of increase in weight. Values of Cre excretion at different stages of recovery expressed in terms of weight or height differed somewhat from those reported by others. The possible significance of these findings is discussed.

3. High correlations of the OHPr index according to Whitehead (1965) determined on 6 h and 24 h collections provided evidence for the representative nature of ‘spot’ samples.

4. Partial correlation analysis of body-weight and urine volume in relation to Cre excretion (mg/24 h) showed that the former (r = 0.719) had a greater influence than the latter (r= 0.485).

5. In a subgroup of eleven marasmic infants aged 3–5 months multiple linear regression analyses of OHPr and Cre excretion on somatic and dietary factors revealed no consistent correlations.

6. Periods of lowered OHPr and Cre excretion were frequent but in only half of the instances were they related to intercurrent infection.

7. A high correlation was found between changes in excretion of OHPr and of Cre throughout recovery.

8. An appraisal was made of the OHPr index according to Whitehead (1965). On the basis of the considerable influence that age was shown to have on this index during the preschool period an OHPr index (age-adjusted) was suggested for use.

9. The OHPr index (age-adjusted) determined on ‘spot’ samples from underprivileged preschool children at home and from marasmic infants during recovery was shown to be closely correlated with a modified ‘index of thriving’ based on somatic measurements.

10. The value of Cre and OHPr determinations in the study of severely malnourished children during recovery and in the detection of mild undernutrition is discussed in the light of these experimental results.

Unhealthy dietary habits can contribute to the development of colorectal cancer (CRC). Such habits may also be associated with post-treatment symptoms experienced by CRC survivors. Therefore, we aimed to assess longitudinal associations of post-treatment unhealthy dietary habits, i.e. intake of ultra-processed foods (UPF), red and processed meat, alcohol and sugar-sweetened drinks, with health-related quality of life (HRQoL), fatigue and chemotherapy-induced peripheral neuropathy (CIPN) in CRC survivors from 6 weeks up to 24 months post-treatment. In a prospective cohort among stage I-III CRC survivors (n 396), five repeated home visits from diagnosis up to 24 months post-treatment were executed. Dietary intake was measured by 7-d dietary records to quantify consumption of UPF, red and processed meat, alcohol and sugar-sweetened drinks. HRQoL, fatigue and CIPN were measured by validated questionnaires. We applied confounder-adjusted linear mixed models to analyse longitudinal associations from 6 weeks until 24 months post-treatment. We applied a post hoc time-lag analysis for alcohol to explore the directionality. Results showed that higher post-treatment intake of UPF and sugar-sweetened drinks was longitudinally associated with worsened HRQoL and more fatigue, while higher intake of UPF and processed meat was associated with increased CIPN symptoms. In contrast, post-treatment increases in alcohol intake were longitudinally associated with better HRQoL and less fatigue; however, time-lag analysis attenuated these associations. In conclusion, unhealthy dietary habits are longitudinally associated with lower HRQoL and more symptoms, except for alcohol. Results from time-lag analysis suggest no biological effect of alcohol; hence, the longitudinal association for alcohol should be interpreted with caution.

Studies have suggested that meal timing plays a role in nutritional health, but this subject has not been sufficiently studied in pregnant women. We analysed the effect that timing of food intake has on eating patterns, diet quality and weight gain in a prospective cohort study with 100 pregnant women. Data were collected once per trimester: 4th–12th, 20th–26th and 30th–37th weeks. Food intake was evaluated using three 24-h dietary recalls, which were used to assess eating patterns and diet quality. Distribution of energy and macronutrient intake throughout the day was considered eating patterns. Diet quality was assessed using the Brazilian Healthy Eating Index-Revised. Weight gain was evaluated during each trimester. Women were classified as early or late timing of the first and last eating episodes if these values were below or above the median of the population, respectively (first eating episode = 08.38 hours; last eating episode = 20.20 hours). Generalised estimating equation models adjusted for confounders were used to determine the effects of timing of the first and last eating episodes (groups) and gestational trimesters (time) (independent variable) on eating patterns, diet quality and weight gain (dependent variables). Early eaters of the first eating episode have a higher percentage of energy and carbohydrate intake in morning and a lower at evening meals. They also have a better diet quality for fruit components when compared with late eaters of the first eating episode. Our results emphasise the importance of considering meal timing in the nutritional antenatal guidelines to promote maternal–fetal health.

Marginally vitamin C-deficient guinea-pigs treated with the diabetogenic agent streptozotocin were compared with those liberally supplied with vitamin C, for functional indices of vitamin C status, particularly in the eye lens. Weanling male Dunkin–Hartley guinea-pigs were fed on diets with 0.1 g vitamin C/kg (marginally deficient), or 5 g/kg (liberally supplied), and some received intraperitoneal streptozotocin (two doses of 150 mg/kg body-weight). About half the streptozotocin-treated animals had high urinary glucose following an oral glucose dose; these animals also grew more slowly than the others. At 4 months after streptozotocin the animals were killed for measurement of tissue vitamin C, glucose and sorbitol. Streptozotocin moderately increased the concentration of glucose in plasma, lens and aqueous humour. Lens sorbitol levels increased only in the group exposed to streptozotocin plus marginal vitamin C. There was a significant (P < 0.02) positive correlation between urinary glucose and lens sorbitol levels overall. Liberal vitamin C intake may thus counteract the effect of streptozotocin diabetes on lens sorbitol, suggesting a new function of vitamin C, possibly related to cataractogenesis and to the biochemical lesions associated with diabetes.

We investigated the associations between dietary patterns and chronic disease mortality in Switzerland using an ecological design and explored their spatial dependence, i.e. the tendency of near locations to present more similar and distant locations to present more different values than randomly expected. Data of the National Nutrition Survey menuCH (n 2057) were used to compute hypothesis- (Alternate Healthy Eating Index (AHEI)) and data-driven dietary patterns. District-level standardised mortality ratios (SMR) were calculated using the Swiss Federal Statistical Office mortality data and linked to dietary data geographically. Quasipoisson regression models were fitted to investigate the associations between dietary patterns and chronic disease mortality; Moran’s I statistics were used to explore spatial dependence. Compared with the first, the fifth AHEI quintile (highest diet quality) was associated with district-level SMR of 0·95 (95 % CI 0·93, 0·97) for CVD, 0·91 (95 % CI 0·88, 0·95) for ischaemic heart disease (IHD), 0·97 (95 % CI 0·95, 0·99) for stroke, 0·99 (95 % CI 0·98, 1·00) for all-cancer, 0·98 (95 % CI 0·96, 0·99) for colorectal cancer and 0·93 (95 % CI 0·89, 0·96) for diabetes. The Swiss traditional and Western-like patterns were associated with significantly higher district-level SMR for CVD, IHD, stroke and diabetes (ranging from 1·02 to 1·08) compared with the Prudent pattern. Significant global and local spatial dependence was identified, with similar results across hypothesis- and data-driven dietary patterns. Our study suggests that dietary patterns partly contribute to the explanation of geographic disparities in chronic disease mortality in Switzerland. Further analyses including spatial components in regression models would allow identifying regions where nutritional interventions are particularly needed.

The present study aimed to investigate the relationships between macronutrient intake and serum lipid profile in adolescents from eight European cities participating in the HELENA (Healthy Lifestyle in Europe by Nutrition in Adolescence) cross-sectional study (2006–7), and to assess the role of body fat-related variables in these associations. Weight, height, waist circumference, skinfold thicknesses, total cholesterol, HDL-cholesterol (HDL-C), LDL-cholesterol, TAG, apoB and apoA1 were measured in 454 adolescents (44 % boys) aged 12·5–17·5 years. Macronutrient intake (g/4180 kJ per d (1000 kcal per d)) was assessed using two non-consecutive 24 h dietary recalls. Associations were evaluated by multi-level analysis and adjusted for sex, age, maternal education, centre, sum of four skinfolds, moderate-to-vigorous physical activity, sedentary behaviours and diet quality index for adolescents. Carbohydrate intake was inversely associated with HDL-C (β = − 0·189, P< 0·001). An inverse association was found between fat intake and TAG (β = − 0·319, P< 0·001). Associations between macronutrient intake and serum lipids varied according to adiposity levels, i.e. an inverse association between carbohydrate intake and HDL-C was only observed in those adolescents with a higher waist:height ratio. As serum lipids and excess body fat are the major markers of CVD, these findings should be considered when developing strategies to prevent the risk of CVD among adolescents.

Mammalian cells accumulate vitamin C either as ascorbic acid (AA), via Na+–AA co-transport, or dehydroascorbic acid (DHA, the oxidation product of AA), via facilitative hexose transport. As the latter, unlike the former, is a high-capacity transport mechanism, cultured cells normally accumulate greater levels of vitamin C when exposed to increasing concentrations of DHA as compared with AA. We report herein similar results using the U937 cell clone used in our laboratory only under conditions in which DHA and AA are used at concentrations greater than 50–60 μm. Below 60 μm, i.e. at levels in which AA is normally found in most biological fluids, AA and DHA are in fact taken up with identical rates and kinetics. Consequently, extracellular oxidation of AA switches the mode of uptake with hardly any effect on the net amount of vitamin C accumulated. As a final note, under these conditions, neither AA nor DHA causes detectable toxicity or any change in the redox status of the cells, as assessed by the reduced glutathione/reduced pyridine nucleotide pool. These findings therefore imply that some cell types do not have a preferential route for vitamin C accumulation, and that the uptake mechanism is uniquely dependent on the extracellular availability of AA v. DHA.

1. Electroencephalographic and nerve-conduction studies were undertaken in children who had been treated in hospital for kwashiorkor 6–8 years previously; the results were compared with those for age-matched controls of similar cultural and socio-economic backgrounds.

2. The electroencephalograms were normal in all.

3. In three survivors of kwashiorkor, the amplitude of the sural nerve potential was less than that of the lower limit of the normal range.

4. The findings are discussed in the context of the present knowledge of protein-energy (protein-calorie) malnutrition.

We aimed to investigate the trends of breast milk lutein concentrations at different times and their relationship with dietary lutein intake during the 12 weeks after delivery. Breast milk samples were collected from thirty-seven mothers at 4, 8 and 12 weeks postpartum. A HPLC detection method was used to measure breast milk lutein concentrations. Dietary intake was assessed using an FFQ, and then dietary lutein intake was calculated. The correlations between dietary lutein intake and breast milk lutein concentrations during lactation were investigated by Pearson’s correlation coefficient. General linear regression models were used to evaluate the optimal regression equation. The mean values of dietary lutein intake at 4, 8 and 12 weeks postpartum were 5·22 (sd 3·60), 7·28 (sd 4·30) and 7·33 (sd 4·24) mg/d, respectively. The mean values of breast milk lutein concentrations at 4, 8 and 12 weeks postpartum were as follows: 46·41 (sd 41·36), 57·96 (sd 40·00) and 62·33 (sd 30·10) μg/l, respectively. Breast milk lutein concentrations were positively associated with dietary lutein intake at 4 weeks postpartum (r 0·527, P < 0·05), which was consistent with the positive correlations observed at 8 and 12 weeks postpartum (r 0·444, P < 0·05; r 0·468, P < 0·05) by the sensitivity analysis. Increased dietary lutein intake can increase the concentration of lutein in the breast milk, and women are recommended to increase their dietary intake of green leafy vegetables and fruits that are rich in lutein during the pregnancy and postpartum periods.

Prompt identification of responders to non-surgical therapy is of utmost importance in attempting medical treatment in patients with clinically severe obesity before indication of bariatric surgery. The objectives of the present study were to assess the outcome at 1 year of morbidly obese patients undergoing a weight-loss medical programme and to detect baseline predictors of a loss ≥10 % of initial weight at the end of the follow-up. A longitudinal, prospective study of a cohort of morbidly obese patients (n 182; females 78 %; age 40·5 (sd 11·5) years; BMI 45·4 (sd 6·0) kg/m2) enrolled in a 1-year obesity-management programme based on lifestyle changes and pharmacological therapy. Significant laboratory and clinical variables were included in a binary logistic regression model in order to identify baseline independent factors for the prediction of a successful outcome in the programme. At 12 months of follow-up, twenty-one subjects (11·5 % of the initial cohort) had lost ≥10 % of baseline weight. A high serum folic acid level was the only independent predictor of weight loss at 1 year. A rise of 1 ng/ml in serum folate increased the chance of success by 28 % (adjusted odds ratio 1·28; 95 % CI 1·04, 1·58). We concluded that a medical-management programme of morbid obesity obtained limited results at 1 year, in agreement with other intervention studies. Serum folate may be useful as a pre-treatment predictor of response to a medical-management programme in patients with morbid obesity. Patients with low basal serum folate levels probably should be urged to change unhealthy eating patterns.

A healthy lifestyle during adolescence is associated with insulin sensitivity or liver enzyme levels and thus might contribute to the prevention of non-alcoholic fatty liver disease (NAFLD). Therefore, we examined the association between adherence to a hypothesis-based lifestyle score including dietary intake, physical activity, sedentary behaviour, sleep duration and BMI in adolescence and fatty liver indices in early adulthood. Overall, 240 participants of the DOrtmund Nutritional and Anthropometric Longitudinally Designed study completed repeated measurements of lifestyle score factors during adolescence (females: 8·5–15·5 years, males: 9·5–16·5 years). Multivariable linear regression models were used to investigate the association between adolescent lifestyle scores and NAFLD risk (hepatic steatosis index (HSI) and fatty liver index (FLI)) in early adulthood (18–30 years). Participants visited the study centre 4·9 times during adolescence and achieved on average 2·8 (min: 0·6, max: 5) out of five lifestyle score points. Inverse associations were observed between the lifestyle score and fatty liver indices (HSI: ß=−5·8 % (95 % CI −8·3, −3·1), P < 0·0001, FLI: ß=−32·4 % (95 % CI −42·9, −20·0), P < 0·0001) in the overall study population. Sex-stratified analysis confirmed these results in men, while inverse but non-significant associations were observed in women (P > 0·05). A higher lifestyle score was associated with lower HSI and FLI values, suggesting that a healthy lifestyle during adolescence might contribute to NAFLD prevention, predominantly in men. Our findings on repeatedly measured lifestyle scores in adolescents and their association with NAFLD risk in early adulthood warrant confirmation in larger study populations.

1.The anthropometric measurements and neurointegrative performance of seventy-nine children aged 6–12 years who had survived kwashiorkor in early childhood were compared to those of 142 children who served as controls.

2. For the boys the differences in height and weight between those who had survived protein-energy malnutrition (PEM) and the controls were significant (P < 0.01).

3. For the girls the differences in height and weight between those who had survived PEM and the controls were not significant.

4. In the tests chosen, the performances of the survivors of PEM was significantly poorer than that of the controls.

5. There was no improvement in the performance when thirteen survivors were reassessed at 10 years of age.

6. There was a significant difference in scholastic performance between the survivors of PEM and the normal controls. The scholastic performance of the siblings of PEM survivors was also significantly better than that of the PEM survivors.

7. The dietary intakes at the time of reassessment were unsatisfactory in 25% of the survivors, but did not relate to their scholastic abilities.

The typical dietary supply of total fat, fatty acids, starch, sugars, polyols and dietary fibre in Sweden was assessed from analyses of market baskets (MB) purchased in 2005 and 2010. MB were based on food balance sheets, with each basket comprising about 130 foods, which represented more than 90 % of annual dietary supply. Foods were divided into ten to twelve categories. In 2010, total fat contributed 34 % of energy (E%), SFA 14·3 E%, MUFA 12·8 E%, PUFA 4·6 E%, n-6 fatty acids 3·6 E%, n-3 fatty acids 1·0 E% and trans-fatty acids (TFA) 0·5 E%. Glycaemic carbohydrates contributed 47 E%, monosaccharides 9 E%, sucrose 11 E%, disaccharides 15 E% and total sugars 24 E%. Added sugars contributed about 15 E%. Dietary fibre content was about 1·7 g/MJ in the 2010 MB. Compared with the 2005 MB, the dietary supply of TFA and dietary fibre was lower, otherwise differences were small. The present MB survey shows that the content of SFA and added sugars was higher than the current Nordic Nutrition Recommendations, while the content of PUFA and especially dietary fibre was lower. TFA levels decreased and dietary supply was well below the recommendations of the WHO. These results emphasise a focus on quality and food sources of fat and carbohydrates, limiting foods rich in SFA and added sugars and replacing them with foods rich in dietary fibre and cis-unsaturated fatty acids.

A Mediterranean-style eating pattern (MED-EP) may include moderate red meat intake. However, it is unknown if the pro-atherogenic metabolite trimethylamine N-oxide (TMAO) is affected by the amount of red meat consumed with a MED-EP. The results presented are from a secondary, retrospective objective of an investigator-blinded, randomised, crossover, controlled feeding trial (two 5-week interventions separated by a 4-week washout) to determine if a MED-EP with 200 g unprocessed lean red meat/week (MED-CONTROL) reduces circulating TMAO concentrations compared to a MED-EP with 500 g unprocessed lean red meat/week (MED-RED). Participants were seventy-seven women and twelve men (n 39 total) who were either overweight or obese (BMI: mean (30·5) (sem 0·3) kg/m2). Serum samples were obtained following an overnight fast both before (pre) and after (post) each intervention. Fasting serum TMAO, choline, carnitine and betaine concentrations were measured using a targeted liquid chromatography-MS. Data were analysed to assess if (a) TMAO and related metabolites differed by intervention and (b) if changes in TMAO were associated with changes in Framingham 10-year risk score. Serum TMAO was lower post-intervention following MED-CONTROL compared with MED-RED intervention (post-MED-CONTROL 3·1 (sem 0·2) µmv. post-MED-RED 5·0 (sem 0·5) µm, P < 0·001), and decreased following MED-CONTROL (pre- v. post-MED-CONTROL, P = 0·025). Exploratory analysis using mixed model ANCOVA identified a positive association between changes in TMAO and changes in homoeostatic model assessment of insulin resistance (P = 0·036). These results suggest that lower amounts of red meat intake lead to lower TMAO concentrations in the context of a MED-EP.

1. The action of vitamin D on the degree of mineralization of the bone tissue of rats given a diet containing adequate amounts of calcium and phosphorus for 8 weeks has been investigated by quantitative microradiography. The method is described.

2. There was a significant reduction in the growth of the vitamin D-deficient rats; the reduction was most marked in the females.

3. Serum analysis showed a reduction in Ca, but P was unchanged. However, the Ca × P product was considered to be high enough to permit normal mineralization.

4. The degree of mineralization of the cortical bone tissue increased significantly according to the distance from the epiphyseal plate. However, there were no significant differences between vitamin D-treated and vitamin D-deficient animals.

5. It is concluded that vitamin D deficiency in rats does not prevent the formation of a bone matrix which can attain a normal degree of mineralization.