Glucagon-like peptide-1 (GLP-1) is an incretin hormone that regulates postprandial glycaemic response by enhancing insulin secretion. We previously demonstrated that the postprandial GLP-1 response was enhanced during the development of diet-induced obesity in rats. However, the physiological relevance of the enhanced GLP-1 response remained unclear. We aimed to determine the role of endogenous GLP-1 during obesity development. Male Sprague–Dawley rats were given either a control diet or a high-fat/high-sucrose (HFS, 30 % fat and 40 % sucrose, weight basis) diet with or without continuous administration of the GLP-1 receptor antagonist, exendin (9–39) (Ex9, 100 µg/d), for 5 weeks. Meal tolerance tests (MTT) were performed to assess postprandial glucose, insulin and GLP-1 responses to a liquid diet administration (15 kcal (63 kJ)/10 ml per kg body weight) every 2 weeks. The AUC of postprandial glucose in the HFS group was similar to the control group in both MTT (P = 0·9665 and P = 0·3475, respectively), whereas AUC of postprandial GLP-1 (after 4 weeks,P = 0·0457) and of insulin (after 2 and 4 weeks, P = 0·0486 and P = 0·0110) was higher in the HFS group compared with the control group. In the Ex9 group, AUC of postprandial glucose (P = 0·0297 and P = 0·0486) was higher along with a lower insulin response compared with the HFS group (P = 0·0564 and P = 0·0281). These results suggest that enhancement of the postprandial GLP-1 response during obesity development has a role in maintaining a normal postprandial glycaemic response. Hence, enhancing endogenous GLP-1 secretion by certain materials could be a potential target for prevention of glucose intolerance.

The present study aimed to determine if the long-chain MUFA cetoleic acid (22 : 1n-11) can improve the capacity to synthesise the health-promoting n-3 fatty acids EPA and DHA in human and fish models. Human hepatocytes (HepG2) and salmon primary hepatocytes were first enriched with cetoleic acid, and thereafter their capacities to convert radio-labelled 18 : 3n-3 (α-linolenic acid, ALA) to EPA and DHA were measured. Increased endogenous levels of cetoleic acid led to increased production of radio-labelled EPA + DHA in HepG2 by 40 % and EPA in salmon hepatocytes by 12 %. In order to verify if dietary intake of a fish oil rich in cetoleic acid would have the same beneficial effects on the n-3 fatty acid metabolic pathway in vivo as found in vitro, Atlantic salmon were fed four diets supplemented with either sardine oil low in cetoleic acid or herring oil high in cetoleic acid at two inclusion levels (Low or High). The diets were balanced for EPA + DHA content within the Low and within the High groups. The salmon were fed these diets from 110 to 242 g. The level of EPA + DHA in liver and whole-body retention of docosapentaenoic acid and EPA + DHA relative to what was eaten, increased with increased dietary cetoleic acid levels. Thus, it is concluded that cetoleic acid stimulated the synthesis of EPA and DHA from ALA in human HepG2 and of EPA in salmon hepatocytes in vitro and increased whole-body retention of EPA + DHA in salmon by 15 % points after dietary intake of cetoleic acid.

Sarcopenia (loss of muscle mass/strength) burdens many older adults – hospitalised older adults being particularly vulnerable. Treating the condition, protein supplementation (PrS) and resistance training (RT) may act synergistically. Therefore, this block-randomised, double-blind, multicentre intervention study, recruiting geriatric patients > 70 years from three medical departments, investigated the effect of PrS combined with RT during hospitalisation and 12 weeks after discharge. Participants were randomly allocated (1:1) to receive PrS (totally 27·5 g whey protein/d, about 2000 kJ/d) or isoenergetic placebo-products (< 1·5 g protein/d) divided into two servings per d to supplement the habitual diet. Both groups were engaged in a standardised, progressive low-intensity RT programme for the lower extremities (hospital: supervised daily/after discharge: self-training 4×/week). From April 2016 to September 2017, 2351 patients were screened, 462 were eligible, and 165 included. Fourteen were excluded and ten dropped out, leaving 141 participants in the intention-to-treat analysis. The average total protein intake during hospitalisation/after discharge was 1·0 (interquartile range (IQR) 0·8, 1·3)/1·1 (IQR 0·9, 1·3) g/kg per d (protein-group) and 0·6 (IQR 0·5, 0·8)/0·9 (IQR 0·6, 1·0) g/kg per d (placebo group). Both groups improved significantly for the primary and secondary endpoints of muscle mass/strength, functional measurements and quality of life, but no additional effect of PrS was seen for the primary endpoint (30-s chair stand test, repetitions, median changes from baseline: (standard test: 0 (IQR 0, 5) (protein group) v. 2 (IQR 0, 6) (placebo group) and modified test: 2 (IQR 0, 5) (protein group) v. 2 (IQR −1, 5) (placebo group)) or any secondary endpoints (Mann–Whitney U tests, P > 0·05). In conclusion, PrS increasing the total protein intake by 0·4 and 0·2 g/kg per d during hospitalisation and after discharge, respectively, does not seem to increase the adaptive response to low-intensity RT in geriatric medical patients.

Physicochemical properties of diets are believed to play a major role in the regulation of digesta transit in the gastrointestinal tract. Starch, being the dominant nutrient in pig diets, strongly influences these properties. We studied transport of digesta solids and liquids through the upper gastrointestinal tract of ninety pigs in a 3 × 3 factorial arrangement. Dietary treatments varied in starch source (barley, maize and high-amylose maize) and form (isolated starch, ground cereal and extruded cereal). Mean retention times (MRT) of digesta solids ranged 129–225 min for the stomach and 86–124 min for the small intestine (SI). The MRT of solids consistently exceeded that of liquids in the stomach, but not in the SI. Solid digesta of pigs fed extruded cereals remained 29–75 min shorter in the stomach compared with pigs fed ground cereals (P < 0·001). Shear stress of whole digesta positively correlated with solid digesta MRT in the stomach (r 0·33, P < 0·001), but not in the SI. The saturation ratio (SR), the actual amount of water in stomach digesta as a fraction of the theoretical maximum held by the digesta matrix, explained more variation in digesta MRT than shear stress. The predictability of SR was hampered by the accumulation of large particles in the stomach. In addition, the water-holding capacity of gelatinised starch leads to a decreased SR of diets, but not of stomach digesta, which was caused by gastric hydrolysis of starch. Both of these phenomena hinder the predictability of gastric retention times based on feed properties.

Although the impact of diet on physical health is an important public health issue, less attention has been devoted to the relationship between nutrition and children’s mental development. The views of parents and teachers about the extent to which diet affects physical and mental development of children were compared in four European countries. An online questionnaire (developed in English and translated) was circulated through a market research agency. Participants were parents or teachers of children aged 4–10 years without learning or behavioural issues. Questionnaires were returned by 1606 parents (401 in England, Germany and Hungary; 403 in Spain) and 403 teachers (100 in each country, except for 103 in Hungary). Teachers were older than parents (35·3 % v. 18·3 % over 45 years; P<0·001) and less likely to smoke (15·9 % v. 26·3 %, P<0·001). There was no difference between the proportions of parents and teachers who felt that a child’s physical development depended very much/extremely (v. moderately/slightly/not at all) on diet (overall 79·8 %). Lower proportions of both groups thought that mental development was very much/extremely influenced by diet (67·4 %). In the regression modelling, believing that physical and mental performance was greatly influenced by diet was significantly and positively associated with living in Hungary, scoring higher on a measure of General Health Interest and (parents only) level of education attained. Differences existed among countries in most views. Lower levels of awareness of the importance of diet for brain development and cognition (compared with physical health outcomes) indicate the potential for educating consumers, especially parents with lower educational attainment.

Obesity phenotypes can be regarded as an indicator of CVD risk factors. The aim of the present study was to determine the prevalence of adolescents with different obesity phenotypes and the role of obesity phenotypes in prediction of the metabolic syndrome (MetS) in adults. For this population-based cohort study, 2159 adolescents aged 11–18 years were included. Subjects were divided into four obesity phenotype groups: metabolically healthy normal weight (MHNW), metabolically healthy obese (MHO), metabolically unhealthy normal weight (MUNW) and metabolically unhealthy obese (MUO). Cox proportional hazard modelling was used to estimate the incidence of the MetS in adults after a median follow-up of 11·3 years. The incidence rate of the MetS in early adulthood was 111·6 (95 % CI 98·7, 126·3) per 10 000 person-years, with higher values in boys (210·1 (95 % CI 183·0, 241·3)), compared with girls (39·7 (95 % CI 30·2, 52·1)). In the age- and adult BMI-adjusted model, the hazard ratio of the MetS in adulthood for boys was 3·33 (95 % CI 2·08, 5·32) among MUO phenotype followed less than 6 years, 1·71 (95 % CI 1·01, 2·90) among MHO, and 2·52 (95 % CI 1·72, 3·68) among MUNW. All associations were attenuated in girls except for MUO phenotype followed less than 6 years (5·72 (95 % CI 2·14, 15·3)). In conclusion, MUNW and MHO phenotypes in boys, but not in girls, and MUO phenotype in both sexes with less than 6 years of follow-up increased the risk of adult MetS compared with MHNW. It seems that lack of obesity at least in boys does not protect them from MetS development in adulthood.

The aim of this work was to study the bioavailability of fatty acids (FA), focusing on n-3 long-chain (LC) PUFA, carried by different molecular lipid species, that is, phospholipids (PL) or TAG, with three formulations based on fish oils or marine PL, providing a similar n-3 LC PUFA amount. The digestive lipolysis was first assessed using an in vitro enzymatic model. Then, intestinal absorption and enterocyte metabolism were investigated in vivo, on male Wistar rats through lymph lipid analysis. The in vitro results showed that the release of n-3 LC PUFA from lipolysis was increased by 48 % when FA were provided as PL rather than TAG. The in vivo results demonstrated that EPA and DHA from both TAG and PL were similarly absorbed and incorporated into lymph lipids. However, DHA was mainly distributed at the sn-1/3 positions of lymph TAG when provided as marine PL, whereas it was equally distributed at the three positions with marine TAG. On the whole, even if the molecular lipid species of n-3 LC PUFA did not greatly modify the in vivo digestion and absorption steps, it modulated the rearrangement of DHA on the glyceride positions of the lymph TAG, which may further impact the DHA metabolic fate and tissue accretion. Consequently, the present study has provided data which may be used to formulate lipid diets rich in DHA in the context of an insufficient consumption of n-3 PUFA in Western countries.

The characterisation of proteome and peptidome of adolescent mothers’ breast milk brings important information to both mother’s and infant’s health; however, it has not been investigated. Bioactive peptides derived from milk proteins have numerous functions. The bioactivity of breast milk peptides includes anti-inflammatory and antimicrobial activities and regulation of gastrointestinal function. We aimed to characterise the proteome and peptidome of mature breast milk of adolescent mothers and investigate whether it is affected by lactational period. We used a combination of electrophoretic and nano-scale LC-quadrupole time-of-flight MS/MS (nLC-Q-TOF-MS/MS) techniques and bioinformatics to explore the proteome of human skimmed milk expressed by lactating adolescents in two groups according to postpartum period (up to 3 and over 5 weeks postpartum). This is the first study that analysed the proteome of adolescent mothers’ breast milk produced during two periods of lactation using 1D-electrophoresis combined with nLC-Q-TOF-MS/MS analysis. Our results showed that the protein composition of adolescent milk varies independently of lactation stage and showed high inter-individual variation. A total of 424 proteins were identified in skimmed milk, of which 137 proteins were common to both groups. Most of the peptides found in adolescents’ breast milk were not derived from major proteins in milk. Association maps showed several interactions between groups of peptides that pointed to the relevance of breast milk peptides to neonatal defensive system.

Some studies found that providing micronutrient powder (MNP) causes adverse health outcomes, but modifying factors are unknown. We aimed to investigate whether Fe status and inherited Hb disorders (IHbD) modify the impact of MNP on growth and diarrhoea among young Lao children. In a double-blind controlled trial, 1704 children of age 6–23 months were randomised to daily MNP (with 6 mg Fe plus fourteen micronutrients) or placebo for about 36 weeks. IHbD, and baseline and final Hb, Fe status and anthropometrics were assessed. Caregivers provided weekly morbidity reports. At enrolment, 55·6 % were anaemic; only 39·3 % had no sign of clinically significant IHbD. MNP had no overall impact on growth and longitudinal diarrhoea prevalence. Baseline Hb modified the effect of MNP on length-for-age (LAZ) (P for interaction = 0·082). Among children who were initially non-anaemic, the final mean LAZ in the MNP group was slightly lower (–1·93 (95 % CI –1·88, –1·97)) v. placebo (–1·88 (95 % CI –1·83, –1·92)), and the opposite occurred among initially anaemic children (final mean LAZ –1·90 (95 % CI –1·86, –1·94) in MNP v. –1·92 (95 % CI –1·88, –1·96) in placebo). IHbD modified the effect on diarrhoea prevalence (P = 0·095). Among children with IHbD, the MNP group had higher diarrhoea prevalence (1·37 (95 % CI 1·17, 1·59) v. 1·21 (95 % CI 1·04, 1·41)), while it was lower among children without IHbD who received MNP (1·15 (95 % CI 0·95, 1·39) v. 1·37 (95 % CI 1·13, 1·64)). In conclusion, there was a small adverse effect of MNP on growth among non-anaemic children and on diarrhoea prevalence among children with IHbD.

For decades, fructose intake has been recognised as an environmental risk for metabolic syndromes and diseases. Here we comprehensively examined the effects of fructose intake on mice liver transcriptomes. Fructose-supplemented water (34 %; w/v) was fed to both male and female C57BL/6N mice at their free will for 6 weeks, followed by hepatic transcriptomics analysis. Based on our criteria, differentially expressed genes (DEG) were selected and subjected to further computational analyses to predict key pathways and upstream regulator(s). Subsequently, predicted genes and pathways from the transcriptomics dataset were validated via quantitative RT-PCR analyses. As a result, we identified eighty-nine down-regulated and eighty-eight up-regulated mRNA in fructose-fed mice livers. These DEG were subjected to bioinformatics analysis tools in which DEG were mainly enriched in xenobiotic metabolic processes; further, in the Ingenuity Pathway Analysis software, it was suggested that the aryl hydrocarbon receptor (AhR) is an upstream regulator governing overall changes, while fructose suppresses the AhR signalling pathway. In our quantitative RT-PCR validation, we confirmed that fructose suppressed AhR signalling through modulating expressions of transcription factor (AhR nuclear translocator; Arnt) and upstream regulators (Ncor2, and Rb1). Altogether, we demonstrated that ad libitum fructose intake suppresses the canonical AhR signalling pathway in C57BL/6N mice liver. Based on our current observations, further studies are warranted, especially with regard to the effects of co-exposure to fructose on (1) other types of carcinogens and (2) inflammation-inducing agents (or even diets such as a high-fat diet), to find implications of fructose-induced AhR suppression.

A number of clinical trials have examined the effect of l-arginine on lipid profile in recent years; however, the results remain equivocal. Therefore, the present study aims to summarise and quantitatively examine the available evidence on the effectiveness l-arginine supplementation on lipid parameters using a systematic review and meta-analytic approach. Online databases including PubMed, Scopus, ISI Web of Science, Cochrane Library and Google Scholar were searched up to April 2019 for randomised controlled trials that examined the effect of l-arginine supplementation on lipid profile in adults. Treatment effects were expressed as weighted mean difference (WMD) and the corresponding standard error in concentrations of serum lipids. To estimate the overall effect of l-arginine supplementation, we used the random-effects model. In total, twelve studies were included in the systematic review. The meta-analysis revealed that l-arginine supplementation did not significantly change the concentrations of total cholesterol (WMD: –5·03 mg/dl; 95 % CI –10·78, 0·73; P = 0·08; inconsistency index (I2) = 39·0 %), LDL (WMD: –0·47 mg/dl; 95 % CI –3·61, 2·66; P = 0·76; I2 = 0·0 %), or HDL (WMD: 0·57 mg/dl; 95 % CI –1·28, 2·43; P = 0·54; I2 = 68·4 %). A significant reduction was observed only in serum TAG levels (WMD: –7·04 mg/dl; 95 % CI –11·42, –2·67; P < 0·001; I2 = 0·0 %). This meta-analysis concludes that l-arginine supplementation can significantly reduce blood TAG levels; however, there is insufficient evidence to support its hypocholesterolaemic effects. To draw straightforward conclusions regarding generalised recommendations for l-arginine supplementation for improving lipid profile, there is a need for more well-controlled trials targeting exclusively patients with dyslipidaemia.

Cancer-related fatigue (CRF) is one of the most commonly reported disease- and treatment-related side effects that impede quality of life. This systematic review and meta-analysis describes the effects of nutrition therapy on CRF and quality of life in people with cancer and cancer survivors. Studies were identified from four electronic databases until September 2017. Eligibility criteria included randomised trials in cancer patients and survivors; any structured dietary intervention describing quantities, proportions, varieties and frequencies of food groups or energy and macronutrient consumption targets; and measures of CRF and quality of life. Standardised mean differences (SMD) were pooled using random-effects models. The American Dietetic Association’s Evidence Analysis Library Quality Checklist for Primary Research was used to evaluate the methodological quality and risk of bias. A total of sixteen papers, of fifteen interventions, were included, comprising 1290 participants. Nutrition therapy offered no definitive effect on CRF (SMD 0·18 (95 % CI –0·02, 0·39)) or quality of life (SMD 0·07 (95 % CI –0·10, 0·24)). Preliminary evidence indicates plant-based dietary pattern nutrition therapy may benefit CRF (SMD 0·62 (95 % CI 0·10, 1·15)). Interventions using the patient-generated subjective global assessment tool and prescribing hypermetabolic energy and protein requirements may improve quality of life. However, the heterogeneity seen in study design, nutrition therapies, quality-of-life measures and cancer types impede definitive dietary recommendations to improve quality of life for cancer patients. There is insufficient evidence to determine the optimal nutrition care plan to improve CRF and/or quality of life in cancer patients and survivors.

When readymade parenteral nutrition in multi-chamber bags is supplied without vitamins and minerals, these have to be added or given separately. Separate rapid infusion has logistical advantages but has been claimed to saturate tissue mechanisms, potentially increasing urine micronutrient losses. The present study compared urinary losses after fast (1 h) v. slow (10 h) trace elements infusion. The study enrolled thirty-nine consecutive patients who were starting parenteral nutrition postoperatively. One day’s dose of a complete intravenous micronutrient product was infused over 1 h and over 10 h, in random order, with a washout day after each infusion day. Urinary Zn, Mn, Se, Cr, Cu and Fe losses were measured by 24-h urine collection, recorded for each infusion day and subsequent washout day. For Zn, a dose of 100 μmol was given, and total urinary loss over the next 2 d was mean 40·6 (sd 23·8) μmol after the fast (1 h) infusion v. 33·4 (sd 25·4) μmol after the slow (10 h) infusion, that is, 7 % more of the 1-d dose was lost after fast infusion (P = 0·01). For Mn, after a dose of 1000 nmol, losses were 9·8 (sd 23·9) nmol after the fast infusion v. 22·1 (sd 47·2) nmol after the slow infusion, that is, 1 % more of the 1-d dose was lost after slow infusion (P = 0·04). There were no other significant differences: after 1 μmol Se, the losses were 1·5 (sd 0·6) μmol fast v. 1·3 (sd 0·5) μmol slow; after 200 nmol Cr, 257 (sd 92) μmol fast v. 246 (sd 107) nmol slow; after 8 μmol Cu, 1·6 (sd 1·4) μmol fast v. 1·5 (sd 1·3) μmol slow; and after 20 μmol Fe, 0·6 (sd 1·1) μmol fast v. 0·8 (sd 1·6) μmol slow (P > 0·05 for all). Overall, trace element retention appears to be minimally affected by infusion time.

This study was performed to evaluate the effects of vitamin D and n-3 fatty acids’ co-supplementation on markers of cardiometabolic risk in diabetic patients with CHD. This randomised, double-blinded, placebo-controlled trial was conducted among sixty-one vitamin D-deficient diabetic patients with CHD. At baseline, the range of serum 25-hydroxyvitamin D levels in study participants was 6·3–19·9 ng/ml. Subjects were randomly assigned into two groups either taking 50 000 IU vitamin D supplements every 2 weeks plus 2× 1000 mg/d n-3 fatty acids from flaxseed oil (n 30) or placebo (n 31) for 6 months. Vitamin D and n-3 fatty acids’ co-supplementation significantly reduced mean (P = 0·01) and maximum levels of left carotid intima–media thickness (CIMT) (P = 0·004), and mean (P = 0·02) and maximum levels of right CIMT (P = 0·003) compared with the placebo. In addition, co-supplementation led to a significant reduction in fasting plasma glucose (β −0·40 mmol/l; 95 % CI −0·77, −0·03; P = 0·03), insulin (β −1·66 μIU/ml; 95 % CI −2·43, −0·89; P < 0·001), insulin resistance (β −0·49; 95 % CI −0·72, −0·25; P < 0·001) and LDL-cholesterol (β −0·21 mmol/l; 95 % CI −0·41, −0·01; P = 0·04), and a significant increase in insulin sensitivity (β +0·008; 95 % CI 0·004, 0·01; P = 0·001) and HDL-cholesterol (β +0·09 mmol/l; 95 % CI 0·01, 0·17; P = 0·02) compared with the placebo. Additionally, high-sensitivity C-reactive protein (β −1·56 mg/l; 95 % CI −2·65, −0·48; P = 0·005) was reduced in the supplemented group compared with the placebo group. Overall, vitamin D and n-3 fatty acids’ co-supplementation had beneficial effects on markers of cardiometabolic risk.

The contribution of milk and dairy products to daily iodine intake is high but variable in many industrialised countries. Factors that affect iodine concentrations in milk and dairy products are only poorly understood. Our aim was to: (1) assess the effect of feed iodine concentration on milk iodine by supplementing five groups of five cows each with one of five dosages from 0–2 mg iodine/kg DM; (2) quantify iodine losses during manufacturing of cheese and yogurt from milk with varying iodine concentrations and assess the effect of cellar-ripening; and (3) systematically measure iodine partitioning during heat treatment and skimming of milk. Milk iodine reached a near-steady state after 3 weeks of feeding. Median milk iodine (17–302 μg/l for 0–2 mg iodine/kg DM) increased linearly with feed iodine (R2 0·96; P < 0·001). At curd separation, 75–84 % of iodine was lost in whey. Dairy iodine increased linearly with milk iodine (semi-hard cheese: R2 0·95; P < 0·001; fresh cheese and yogurt: R2 1·00; P < 0·001), and cellar-ripening had no effect. Heat treatment had no significant effect, whereas skimming increased (P < 0·001) milk iodine concentration by only 1–2 μg/l. Mean daily intake of dairy products by Swiss adults is estimated at 213 g, which would contribute 13–52 % of the adults’ RDA for iodine if cow feed is supplemented with 0·5–2 mg iodine/kg DM. Thus, modulation of feed iodine levels can help achieve desirable iodine concentrations in milk and dairy products, and thereby optimise their contribution to human iodine nutrition to avoid both deficiency and excess.

We aimed to investigate the association between plasma retinol and incident cancer among Chinese hypertensive adults. We conducted a nested case–control study, including 231 patients with incident cancer and 231 matched controls during a median 4·5-year follow-up of the China Stroke Primary Prevention Trial. There was a significant, inverse association between retinol levels and digestive system cancer (per 10 μg/dl increases: OR 0·79; 95 % CI 0·69, 0·91). When compared with participants in the first quartile of retinol (< 52·3 μg/dl), a significantly lower cancer risk was found in participants in quartile 2–4 ( ≥ 52·3 μg/dl: OR 0·31; 95 % CI 0·13, 0·71). However, there was a U-shaped association between retinol levels and non-digestive system cancers where the risk of cancers decreased (although not significantly) with each increment of plasma retinol (per 10 μg/dl increases: OR 0·89; 95 % CI 0·60, 1·31) in participants with retinol < 68·2 μg/dl, and then increased significantly with retinol (per 10 μg/dl increase: OR 1·65; 95 % CI 1·12, 2·44) in participants with retinol ≥ 68·2 μg/dl. In conclusion, there was a significant inverse dose–response association between plasma retinol and the risk of digestive system cancers. However, a U-shaped association was observed between plasma retinol and the risk of non-digestive cancers (with a turning point approximately 68·2 μg/dl).

Breast-feeding is the ideal nutrition for a newborn’s integral necessities. It seems crucial therefore to know its composition in order to provide suitable infant formula when required. Of these, polyamines (with lactation and the microbiota being its intestinal source) are involved in the development of gut epithelium and immunity. Safety concerns limit human intervention studies. Therefore, we studied the amounts of polyamines supplied by breast milk (varying among mothers) or infant formula feeding, up to day 30 postpartum, in the faeces of newborns. Independent samples (68) of breast milk from fifty-nine healthy Caucasian woman (day 0, 1, 3, 5, 7, 15 and 30 postpartum) who had natural deliveries after week 38, same-day faeces of newborns when available (eighty-one from breast milk and fifty-five from infant formula fed) and six infant formulas were collected and the polyamine content was determined by HPLC. In breast milk, polyamines and isoamylamine (a primary amine), with inter-individual variations, increased over time (with a higher content of spermidine; no other amines were present). Overall, they were much higher than in infant formula. By the 2nd week after birth, polyamines, cadaverine and tyramine, but not isoamylamine, were higher in the faeces of those fed infant formula compared with those fed breast milk. Cadaverine and tyramine could be used to predict the feeding type used for newborns. The differences in the content may be related to distinct colonisation of amine-producing bacteria, which can be established by polyamines. Further studies are required to determine the clinical utility of these findings.

Head circumference in infants has been reported to predict brain size, total grey matter volume (GMV) and neurocognitive development. However, it is unknown whether it has predictive value on regional and subcortical brain volumes. We aimed to explore the relationship between several head circumference measurements since birth and distributions of GMV and subcortical volumes at later childhood. We examined seventy-four, Caucasian, singleton, term-born infants born to mothers randomised to receive fish oil and/or 5-methyltetrahydrofolate or placebo prenatal supplementation. We assessed head circumference at birth and at 4 and 10 years of age and cognitive abilities at 7 years of age. We obtained brain MRI at 10 years of age, on which we performed voxel-based morphometry, cortical surface extraction and subcortical segmentation. Analyses were controlled for sex, age, height, weight, family status, laterality and total intracranial volume. Prenatal supplementation did not affect head circumference at any age, cognitive abilities or total brain volumes. Head circumference at 4 years presented the highest correlation with total GMV, white matter volume and brain surface area, and was also strongly associated with GMV of frontal, temporal and occipital areas, as well as with caudate nucleus, globus pallidus, putamen and thalamus volumes. As relationships between brain volumes in childhood and several outcomes extend into adulthood, we have found that ages between 0 and 4 years as the optimal time for brain growth; postnatal factors might have the most relevant impact on structural maturation of certain cortical areas and subcortical nuclei, independent of prenatal supplementation.

We evaluated the effects of high-Ca fat-free milk v. low-Ca control diet on adiposity and on glycaemic control. Fourteen subjects with type 2 diabetes (aged 49·5 (sd 8·6) years, BMI 29·4 (sd 4·5) kg/m2, low habitual Ca consumption (<600 mg/d)) were included in this randomised, crossover clinical trial. Subjects participated in two 12-week experimental sessions (high-Ca fat-free milk (HC) or low-Ca control (LC)) separated by 8-week washout. Subjects daily consumed in the laboratory a breakfast shake containing 700 mg (HC) or 6·4 mg (LC) of Ca. Energy-restricted diets containing 800 mg of dietary Ca/d were prescribed. Dietary records data indicated the consumption of 1200 mg of Ca/d during HC and of 525 mg of Ca/d during LC. There was a greater reduction in body weight, body fat mass, waist circumference and waist:hip ratio after HC. Serum 25-hydoxyvitamin D and homeostatic model assessment-2 β-cell function (HOMA2-%B) increased, and serum uric acid, parathormone (PTH) and glycated Hb (HbA1c) concentrations reduced after HC. In addition, changes from baseline in terms of serum uric acid, glucose, HbA1c and PTH concentrations were lower, and those of HOMA2-%B, serum Ca and 25-hydoxyvitamin D were higher after the HC than after LC. The consumption of approximately three servings of fat-free milk and 1200 mg of dietary Ca/d enhanced weight loss, improved body composition and promoted glycaemic control in subjects with type 2 diabetes and low habitual Ca consumption (<600 mg/d).

A few studies have recently reported that higher cardiorespiratory fitness is associated with higher volumes of subcortical brain structures in children. It is, however, unknown how different fitness measures relate to shapes of subcortical brain nuclei. We aimed to examine the association of the main health-related physical fitness components with shapes of subcortical brain structures in a sample of forty-four Spanish children aged 9·7 (sd 0·2) years from the NUtraceuticals for a HEALthier life project. Cardiorespiratory fitness, muscular strength and speed agility were assessed using valid and reliable tests (ALPHA-fitness test battery). Shape of the subcortical brain structures was assessed by MRI, and its relationship with fitness was examined after controlling for a set of potential confounders using a partial correlation permutation approach. Our results showed that all physical fitness components studied were significantly related to the shapes of subcortical brain nuclei. These associations were both positive and negative, indicating that a higher level of fitness in childhood is related to both expansions and contractions in certain regions of the accumbens, amygdala, caudate, hippocampus, pallidum, putamen and thalamus. Cardiorespiratory fitness was mainly associated with expansions, whereas handgrip was mostly associated with contractions in the structures studied. Future randomised-controlled trials will confirm or contrast our findings, demonstrating whether changes in fitness modify the shapes of brain structures and the extent to which those changes influence cognitive function.