Coconut, Cocos nucifera L., is a tree that is cultivated to provide a large number of products, although it is mainly grown for its nutritional and medicinal values. Coconut oil, derived from the coconut fruit, has been recognised historically as containing high levels of saturated fat; however, closer scrutiny suggests that coconut should be regarded more favourably. Unlike most other dietary fats that are high in long-chain fatty acids, coconut oil comprises medium-chain fatty acids (MCFA). MCFA are unique in that they are easily absorbed and metabolised by the liver, and can be converted to ketones. Ketone bodies are an important alternative energy source in the brain, and may be beneficial to people developing or already with memory impairment, as in Alzheimer's disease (AD). Coconut is classified as a highly nutritious ‘functional food’. It is rich in dietary fibre, vitamins and minerals; however, notably, evidence is mounting to support the concept that coconut may be beneficial in the treatment of obesity, dyslipidaemia, elevated LDL, insulin resistance and hypertension – these are the risk factors for CVD and type 2 diabetes, and also for AD. In addition, phenolic compounds and hormones (cytokinins) found in coconut may assist in preventing the aggregation of amyloid-β peptide, potentially inhibiting a key step in the pathogenesis of AD. The purpose of the present review was to explore the literature related to coconut, outlining the known mechanistic physiology, and to discuss the potential role of coconut supplementation as a therapeutic option in the prevention and management of AD.

The impairment in the rate of cell proliferation and differentiation leads to a negative consequence on the renewal of the intestinal epithelium, which is the aetiological factor of a number of digestive diseases. Grape seed extract (GSE), a rich source of proanthocyanidins, is known for its beneficial health effects. The present study evaluated the beneficial effects of GSE on colonic cell differentiation and barrier function in IL10-deficient mice. Female mice aged 6 weeks were randomised into two groups and given drinking-water containing 0 or 0·1 % GSE (w/v) for 12 weeks. GSE supplementation decreased serum TNF-α level and intestinal permeability, and increased the colonic goblet cell density that was associated with increased mRNA expression of mucin (Muc)-2. Immunohistochemical analyses showed lower accumulation of β-catenin in the crypts of colon tissues of the GSE-supplemented mice, which was associated with a decreased mRNA expression of two downstream effectors of Wingless and Int (Wnt)/catenin signalling, myelocytomatosis oncogene protein (Myc) and cyclin D1 (Ccnd1). Consistently, GSE supplementation decreased the number of colonic proliferating cell nuclear antigen-positive cells, a well-known cell proliferation marker, and a weakened extracellular signal-regulated kinases 1 and 2 (ERK1/2) signalling. In summary, these data indicate that supplementation of 0·1 % GSE for 12 weeks improved gut barrier function and colonic cell differentiation in the IL10-deficient mice probably via inhibiting Wnt/β-catenin pathway.

Adequate dietary iodine intake in children is essential for optimal physical and neurological development. Whether lower dietary animal food and salt intake may adversely affect iodine status is under discussion. We examined the association between dietary animal:plant protein ratio with 24-h urinary iodine excretion (24-h UI, μg/d), and whether this is modified by salt intake. A 24-h UI was measured in 1959 24-h urine samples from 516 6- to 12-year-old participants of the Dortmund Nutritional and Anthropometric Longitudinally Designed Study. Parallel 3 d weighed food records were used to estimate dietary intakes. Protein sources were classified as dairy, animal and plant. A repeated-measures regression model (PROC MIXED) was used to analyse the effect of animal:plant protein ratios on 24-h UI. Animal:plant protein ratios ranged from 0·5 (95 % CI 0·4, 0·6) to 1·6 (95 % CI 1·4, 1·9) (lowest and highest quartile). After adjustment for total energy intake, main dietary iodine sources (dairy and salt intake), and further covariates, the inter-individual variation in animal:plant protein ratio was significantly associated with variation in 24-h UI. One unit higher animal:plant protein ratio predicted 6 μg/d higher 24-h UI (P= 0·002) in boys and 5 μg/d (P= 0·03) in girls. This relationship was partially mediated by a higher salt intake at higher animal:plant protein ratios. These results suggest that lower consumption of animal protein is associated with a small decline in iodine excretion, partially mediated by decreased salt intake. Because limited salt and increased intake of plant-based foods are part of a preferable healthy food pattern, effective nutrition political strategies will be required in the future to ensure appropriate iodine nutrition in adherent populations.

Glucagon-like peptide-1 (GLP-1), which is produced and released from enteroendocrine L cells, plays pivotal roles in postprandial glycaemia. The ingestion of resistant maltodextrin (RMD), a water-soluble non-digestible saccharide, improves the glycaemic response. In the present study, we examined whether the continuous feeding of RMD to rats affected GLP-1 levels and glycaemic control. Male Sprague–Dawley rats (6 weeks of age) were fed an American Institute of Nutrition (AIN)-93G-based diet containing either cellulose (5 %) as a control, RMD (2·5 or 5 %), or fructo-oligosaccharides (FOS, 2·5 or 5 %) for 7 weeks. During the test period, an intraperitoneal glucose tolerance test (IPGTT) was performed after 6 weeks. Fasting GLP-1 levels were significantly higher in the 5 % RMD group than in the control group after 6 weeks. The IPGTT results showed that the glycaemic response was lower in the 5 % RMD group than in the control group. Lower caecal pH, higher caecal tissue and content weights were observed in the RMD and FOS groups. Proglucagon mRNA levels were increased in the caecum and colon of both RMD and FOS groups, whereas caecal GLP-1 content was increased in the 5 % RMD group. In addition, a 1 h RMD exposure induced GLP-1 secretion in an enteroendocrine L-cell model, and single oral administration of RMD increased plasma GLP-1 levels in conscious rats. The present study demonstrates that continuous ingestion of RMD increased GLP-1 secretion and production in normal rats, which could be stimulated by its direct and indirect (enhanced gut fermentation) effects on GLP-1-producing cells, and contribute to improving glucose tolerance.

Immune function changes with ageing and is influenced by physical activity (strength training, ST) and diet (fish oil, FO). The present study investigated the effect of FO and ST on the immune system of elderly women. Forty-five women (64 (sd 1·4) years) were assigned to ST for 90 d (ST; n 15), ST plus 2 g/d FO for 90 d (ST90; n 15) or 2 g/d FO for 60 d followed by ST plus FO for 90 d (ST150; n 15). Training was performed three times per week, for 12 weeks. A number of innate (zymosan phagocytosis, lysosomal volume, superoxide anion, peroxide of hydrogen) and adaptive (cluster of differentiation 4 (CD4), CD8, TNF-α, interferon-γ (IFN-γ), IL-2, IL-6 and IL-10 produced by lymphocytes) immune parameters were assessed before supplementation (base), before (pre-) and after (post-) training. ST induced no immune changes. FO supplementation caused increased phagocytosis (48 %), lysosomal volume (100 %) and the production of superoxide anion (32 %) and H2O2 (70 %) in the ST90. Additional FO supplementation (ST150) caused no additive influence on the immune system, as ST150 and ST90 did not differ, but caused greater changes when compared to the ST (P< 0·05). FO increased CD4+ and CD8+ lymphocytes in the ST150, which remained unchanged when training was introduced. The combination of ST and FO reduced TNF-α in the ST150 from base to post-test. FO supplementation (ST150, base–pre) when combined with exercise (ST150, pre–post) increased IFN-γ, IL-2, IL-6 and IL-10 production. The immune parameters improved in response to FO supplementation; however, ST alone did not enhance the immune system.

Postnatal rapid growth by excess intake of nutrients has been associated with an increased susceptibility to diseases in neonates with intra-uterine growth restricted (IUGR). The aim of the present study was to determine whether postnatal nutritional restriction could improve intestinal development and immune function of neonates with IUGR using piglets as model. A total of twelve pairs of normal-birth weight (NBW) and IUGR piglets (7 d old) were randomly assigned to receive adequate nutrient intake or restricted nutrient intake (RNI) by artificially liquid feeding for a period of 21 d. Blood samples and intestinal tissues were collected at necropsy and were analysed for morphology, digestive enzyme activities, immune cells and expression of innate immunity-related genes. The results indicated that both IUGR and postnatal nutritional restriction delayed the growth rate during the sucking period. Irrespective of nutrient intake, piglets with IUGR had a significantly lower villous height and crypt depth in the ileum than the NBW piglets. Moreover, IUGR decreased alkaline phosphatase activity while enhanced lactase activity in the jejunum and mRNA expressions of Toll-like receptor 9 (TLR-9) and DNA methyltransferase 1 (DNMT1) in the ileum of piglets. Irrespective of body weight, RNI significantly decreased the number and/or percentage of peripheral leucocytes, lymphocytes and monocytes of piglets, whereas the percentage of neutrophils and the ratio of CD4+ to CD8+ were increased. Furthermore, RNI markedly enhanced the mRNA expression of TLR-9 and DNMT1, but decreased the expression of NOD2 and TRAF-6 in the ileum of piglets. In summary, postnatal nutritional restriction led to abnormal cellular and innate immune response, as well as delayed the growth and intestinal development of IUGR piglets.

Some lipid hydrolysis products such as medium-chained NEFA (MC-NEFA), sphingosine and monoacylglycerols (MAG) possess antibacterial activity, while others, including oleic acid, are essential for the optimal growth of Lactobacillus species. Thus, changes in the concentrations of NEFA and MAG in the distal ileum and colon can potentially selectively modulate the composition of the gut microbiota, especially in early life when lipid absorption efficacy is reduced. As medium-chained fatty acids are enriched in mothers' milk, such effects may be highly relevant during gut colonisation. In the present study, we examined the effect of selected NEFA, MAG and sphingosine on the composition of faecal microbial communities derived from infants aged 2–5 months during a 24 h anaerobic in vitro fermentation. We tested lipid mixtures in the concentration range of 0–200 μm, either based on MC-NEFA (10 : 0 to 14 : 0 and MAG 12 : 0) or long-chained NEFA (LC-NEFA; 16 : 0 to 18 : 1 and MAG 16 : 0) with and without sphingosine, representing lipid hydrolysis products characteristic for intestinal hydrolysis of breast milk lipids. Ion Torrent sequencing of the bacterial 16S ribosomal RNA gene revealed that the relative abundance of lactic acid-producing genera, including Lactobacillus and Bifidobacterium, was generally increased in the presence of 50 μm or higher concentrations of MC-NEFA. For Bifidobacterium, the same effect was also observed in the presence of a mixture containing LC-NEFA with sphingosine. On the contrary, the relative abundance of Enterobacteriaceae was significantly decreased in the presence of both lipid mixtures. Our findings suggest that the high concentration of medium-chained fatty acids in breast milk might have functional effects on the establishment of the gut microbiota in early life.

The leaves of the olive plant (Olea europaea) are rich in polyphenols, of which oleuropein and hydroxytyrosol (HT) are most characteristic. Such polyphenols have been demonstrated to favourably modify a variety of cardiovascular risk factors. The aim of the present intervention was to investigate the influence of olive leaf extract (OLE) on vascular function and inflammation in a postprandial setting and to link physiological outcomes with absorbed phenolics. A randomised, double-blind, placebo-controlled, cross-over, acute intervention trial was conducted with eighteen healthy volunteers (nine male, nine female), who consumed either OLE (51 mg oleuropein; 10 mg HT), or a matched control (separated by a 4-week wash out) on a single occasion. Vascular function was measured by digital volume pulse (DVP), while blood collected at baseline, 1, 3 and 6 h was cultured for 24 h in the presence of lipopolysaccharide in order to investigate effects on cytokine production. Urine was analysed for phenolic metabolites by HPLC. DVP-stiffness index and ex vivo IL-8 production were significantly reduced (P< 0·05) after consumption of OLE compared to the control. These effects were accompanied by the excretion of several phenolic metabolites, namely HT and oleuropein derivatives, which peaked in urine after 8–24 h. The present study provides the first evidence that OLE positively modulates vascular function and IL-8 production in vivo, adding to growing evidence that olive phenolics could be beneficial for health.

The majority of neural tube defects were believed to be folic acid (FA)-preventable in the 1990s. The Japanese government recommended women planning pregnancy to take FA supplements of 400 μg/d in 2000, but the incidence of spina bifida has not decreased. We aimed to evaluate the OR of having an infant with spina bifida for women who periconceptionally took FA supplements and the association between an increase in supplement use and possible promoters for the increase. This is a case–control study which used 360 case women who gave birth to newborns afflicted with spina bifida, and 2333 control women who gave birth to healthy newborns during the first 12 years of this century. They were divided into two 6-year periods; from 2001 to 2006 and from 2007 to 2012. Logistic regression analyses were conducted to compute OR between cases and controls. The adjusted OR of having an infant with spina bifida for supplement users was 0·48 in the first period, and 0·53 in the second period. The proportion of women who periconceptionally consumed supplements significantly increased from 10 % in the first period to 30 % in the second period. Awareness of the preventive role of FA was a promoter for an increase in supplement use, and thus an FA campaign in high school seems rational and effective. The failure of the current public health policy is responsible for an epidemic of spina bifida. Mandatory food fortification with FA is urgent and long overdue in Japan.

Phyto-oestrogens are a family of plant-derived xeno-oestrogens that appear to have beneficial effects on human health. To date, no data are available about phyto-oestrogen consumption affecting liver health in a population. The present study aimed to explore the relationship of urinary phyto-oestrogen metabolites with serum liver enzymes in US adults. A nationally representative sample of US adults in the National Health and Nutrition Examination Survey (NHANES) 2003–10 was analysed. The cross-sectional study sample consisted of 6438 adults with data on urinary phyto-oestrogen levels, serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP) and γ-glutamyl transaminase (GGT) concentrations and data on other potential confounders. Multivariate logistic regression and linear regression were applied to assess associations between urinary phyto-oestrogen levels and ALT, AST, ALP and GGT concentrations. We found a remarkable association between urinary enterolactone and GGT in both adult males (OR 0·37, 95 % CI 0·22, 0·61; P= 0·003) and females (OR 0·37, 95 % CI 0·26, 0·54; P= 0·009). Moreover, elevated enterolactone levels were inversely associated with ALT and AST levels in adult males. However, no association was present between levels of urinary daidzein, O-desmethylangolensin, equol, enterodiol or genistein with liver enzyme levels in this population. The present study results provide epidemiological evidence that urinary enterolactone levels are associated with liver GGT levels in humans. This suggests a potential protective effect of enterolactone on human liver function. However, the underlying mechanisms still need further investigation.

Breakfast omission is associated with obesity and CVD/diabetes, but the acute effects of extended morning fasting upon subsequent energy intake and metabolic/hormonal responses have received less attention. In a randomised cross-over design, thirty-five lean men (n 14) and women (n 21) extended their overnight fast or ingested a typical carbohydrate-rich breakfast in quantities relative to RMR (i.e. 1963 (sd 238) kJ), before an ad libitum lunch 3 h later. Blood samples were obtained hourly throughout the day until 3 h post-lunch, with subjective appetite measures assessed. Lunch intake was greater following extended fasting (640 (sd 1042) kJ, P< 0·01) but incompletely compensated for the omitted breakfast, with total intake lower than the breakfast trial (3887 (sd 1326) v. 5213 (sd 1590) kJ, P< 0·001). Systemic concentrations of peptide tyrosine–tyrosine and leptin were greater during the afternoon following breakfast (both P< 0·05) but neither acylated/total ghrelin concentrations were suppressed by the ad libitum lunch in the breakfast trial, remaining greater than the morning fasting trial throughout the afternoon (all P< 0·05). Insulin concentrations were greater during the afternoon in the morning fasting trial (all P< 0·01). There were no differences between trials in subjective appetite during the afternoon. In conclusion, morning fasting caused incomplete energy compensation at an ad libitum lunch. Breakfast increased some anorectic hormones during the afternoon but paradoxically abolished ghrelin suppression by the second meal. Extending morning fasting until lunch altered subsequent metabolic and hormonal responses but without greater appetite during the afternoon. The present study clarifies the impact of acute breakfast omission and adds novel insights into second-meal metabolism.

Iodine is a key component of the thyroid hormones, which are critical for healthy growth, development and metabolism. The UK population is now classified as mildly iodine-insufficient. Adequate levels of iodine during pregnancy are essential for fetal neurodevelopment, and mild iodine deficiency is linked to developmental impairments. In the absence of prophylaxis in the UK, awareness of nutritional recommendations during pregnancy would empower mothers to make the right dietary choices leading to adequate iodine intake. The present study aimed to: estimate mothers' dietary iodine intake in pregnancy (using a FFQ); assess awareness of the importance of iodine in pregnancy with an understanding of existing pregnancy dietary and lifestyle recommendations with relevance for iodine; examine the level of confidence in meeting adequate iodine intake. A cross-sectional survey was conducted and questionnaires were distributed between August 2011 and February 2012 on local (Glasgow) and national levels (online electronic questionnaire); 1026 women, UK-resident and pregnant or mother to a child aged up to 36 months participated in the study. While self-reported awareness about general nutritional recommendations during pregnancy was high (96 %), awareness of iodine-specific recommendations was very low (12 %), as well as the level of confidence of how to achieve adequate iodine intake (28 %). Median pregnancy iodine intake, without supplements, calculated from the FFQ, was 190 μg/d (interquartile range 144–256μg/d), which was lower than that of the WHO's recommended intake for pregnant women (250 μg/d). Current dietary recommendations in pregnancy, and their dissemination, are found not to equip women to meet the requirements for iodine intake.

The aim of this study was to estimate the association between birth order and number of siblings with body composition in adolescents. Data are from a birth cohort study conducted in Pelotas, Brazil. At the age of 18 years, 4563 adolescents were located, of whom 4106 were interviewed (follow-up rate 81·3 %). Of these, 3974 had complete data and were thus included in our analysis. The variables used in the analysis were measured during the perinatal period, or at 11, 15 and/or 18 years of age. Body composition at 18 years was collected by air displacement plethysmography (BOD POD®). Crude and adjusted analyses of the association between birth order and number of siblings with body composition were performed using linear regression. All analyses were stratified by the adolescent sex. The means of BMI, fat mass index and fat-free mass index among adolescents were 23·4 (sd 4·5) kg/m2, 6·1 (sd 3·9) kg/m2 and 17·3 (sd 2·5) kg/m2, respectively. In adjusted models, the total siblings remained inversely associated with fat mass index (β = − 0·37 z-scores, 95 % CI − 0·52, − 0·23) and BMI in boys (β = − 0·39 z-scores, 95 % CI − 0·55, − 0·22). Fat-free mass index was related to the total siblings in girls (β = 0·06 z-scores, 95 % CI − 0·04, 0·17). This research has found that number of total siblings, and not birth order, is related to the fat mass index, fat-free mass index and BMI in adolescents. It suggests the need for early prevention of obesity or fat mass accumulation in only children.

Sufficient iodine intake by pregnant and lactating women is crucial to their offspring's cognitive development. The aim of the present study was to explore the impact of iodised salt intake on the iodine status of pregnant and lactating women. Thirty towns were selected from 211 towns in the rural areas of Shijiazhuang city using probability proportionate to size sampling in this cross-sectional survey. In each selected town, forty pregnant women and forty lactating women were randomly selected to contribute urine samples to determine iodine content. The median urinary iodine content (UIC) of 1200 pregnant women in all was 146 (interquartile range (IQR) 88–239) μg/l. The median UIC in the first, second and third trimesters were 166 (IQR 92–276) μg/l, 145 (IQR 83–248) μg/l and 134 (IQR 79–221) μg/l, respectively. The median UIC in the first trimester was significantly higher than that in the third trimester (P= 0·04). The median UIC of 1200 lactating women in all was 120 (IQR 66–195) μg/l. Their median UIC in every 4-week block was higher than the WHO criteria except in weeks 25–28 and weeks 33–36 of lactation. Pregnant women's median UIC did not correlate with median salt iodine (MSI) (P= 0·402); however, there was a linear correlation between MSI and the lactating women's median UIC (P= 0·007). Iodised salt failed to provide adequate iodine to pregnant women possibly due to limited intake of iodised salt during pregnancy, though it was found to provide adequate iodine to lactating women in the rural areas of Shijiazhuang city.

For cancer prevention, the World Cancer Research Fund and American Institute for Cancer Research (WCRF/AICR) emphasise recommendations to improve individual behaviour, including avoidance of tobacco products, maintaining a lean body mass, participating in physical activity, consuming a plant-based diet, and minimising the consumption of energy-dense foods, such as sodas, red and processed meats and alcohol. In the present study of 275 healthy premenopausal women, we explored the association of adherence scores with levels of three biomarkers of antioxidant and inflammation status: serum C-reactive protein (CRP), serum γ-tocopherol and urinary F2-isoprostane. The statistical analysis applied linear regression across categories of adherence to WCRF/AICR recommendations. Overall, seventy-two women were classified as low ( ≤ 4), 150 as moderate (5–6), and fifty-three as high adherers ( ≥ 7). The unadjusted means for CRP were 2·7, 2·0 and 1·7 mg/l for low, moderate and high adherers (Ptrend= 0·03); this association was strengthened after adjustment for confounders (Ptrend= 0·006). The respective values for serum γ-tocopherol were 1·97, 1·63 and 1·45 μg/ml (Ptrend= 0·02 before and Ptrend= 0·03 after adjustment). Only for urinary F2-isoprostane, the lower values in high adherers (16·0, 14·5, and 13·3 ng/ml) did not reach statistical significance (Ptrend= 0·18). In an analysis by BMI, overweight and obese women had higher biomarker levels than normal weight women; the trend was significant for CRP (Ptrend< 0·001) and γ-tocopherol (Ptrend= 0·003) but not for F2-isoprostane (Ptrend= 0·14). These findings suggest that both adherence to the WCRF/AICR guidelines and normal BMI status are associated with lower levels of biomarkers that indicate oxidative stress and inflammation.

Vitamin D plays an important role in skeletal health throughout life. Some studies have hypothesised that vitamin D may reduce the risk of other diseases. Our study aimed to estimate age-specific and sex-specific serum 25-hydroxyvitamin D (25(OH)D) status and to identify the determinants of serum 25(OH)D status in Hong Kong, a subtropical city in southern China. In 2009–2010, households in Hong Kong were followed up to identify acute respiratory illnesses, and sera from 2694 subjects were collected in three to four different study phases to permit measurement of 25(OH)D levels at different times of the year. A questionnaire survey on diet and lifestyle was conducted among children, with simultaneous serum collection in April and May 2010. The mean of serum 25(OH)D levels in age groups ranged from 39 to 63 nmol/l throughout the year with the mean values in all age groups in spring below 50 nmol/l. Children aged 6–17 years, and girls and women had significantly lower serum 25(OH)D levels than adults, and boys and men, respectively (all P< 0·001). We estimated that serum 25(OH)D levels in Hong Kong followed a lagged pattern relative to climatic season by 5 weeks with lowest observed levels in early spring (March). For children aged 6–17 years, reporting a suntan, having at least 1 servings of fish/week and having at least 1 serving of eggs/week were independently associated with higher serum 25(OH)D levels. Adequate sunlight exposure and increased intake of dietary vitamin D could improve vitamin D status, especially for children and females in the winter and spring.

Diet and inflammation have been suggested to be important risk factors for colorectal cancer (CRC). In the present study, we examined the association between the dietary inflammatory index (DII) and the risk of CRC in a multi-centre case–control study conducted between 1992 and 1996 in Italy. The study included 1225 incident colon cancer cases, 728 incident rectal cancer cases and 4154 controls hospitalised for acute non-neoplastic diseases. The DII was computed based on dietary intake assessed using a validated seventy-eight-item FFQ that included assessment of alcohol intake. Logistic regression models were used to estimate the OR adjusted for age, sex, study centre, education, BMI, alcohol drinking, physical activity and family history of CRC. Energy intake was adjusted using the residual method. Subjects with higher DII scores (i.e. with a more pro-inflammatory diet) had a higher risk of CRC, with the DII being used both as a continuous variable (ORcontinuous 1·13, 95 % CI 1·09, 1·18) and as a categorical variable (ORquintile 5 v. 1 1·55, 95 % CI 1·29, 1·85; P for trend < 0·0001). Similar results were observed when the analyses were carried out separately for colon and rectal cancer cases. These results indicate that a pro-inflammatory diet is associated with an increased risk of CRC.