Metabolic diversity leads to differences in nutrient requirements and responses to diet and medication between individuals. Using the concept of metabotyping – that is, grouping metabolically similar individuals – tailored and more efficient recommendations may be achieved. The aim of this study was to review the current literature on metabotyping and to explore its potential for better targeted dietary intervention in subjects with and without metabolic diseases. A comprehensive literature search was performed in PubMed, Google and Google Scholar to find relevant articles on metabotyping in humans including healthy individuals, population-based samples and patients with chronic metabolic diseases. A total of thirty-four research articles on human studies were identified, which established more homogeneous subgroups of individuals using statistical methods for analysing metabolic data. Differences between studies were found with respect to the samples/populations studied, the clustering variables used, the statistical methods applied and the metabotypes defined. According to the number and type of the selected clustering variables, the definitions of metabotypes differed substantially; they ranged between general fasting metabotypes, more specific fasting parameter subgroups like plasma lipoprotein or fatty acid clusters and response groups to defined meal challenges or dietary interventions. This demonstrates that the term ‘metabotype’ has a subjective usage, calling for a formalised definition. In conclusion, this literature review shows that metabotyping can help identify subgroups of individuals responding differently to defined nutritional interventions. Targeted recommendations may be given at such metabotype group levels. Future studies should develop and validate definitions of generally valid metabotypes by exploiting the increasingly available metabolomics data sets.

This study aimed to explore the potential associations of adherence to the Mediterranean diet with gut microbiota characteristics and gastrointestinal symptomatology in an adult population. Other long-term dietary habits (e.g. consumption of snacks and junk food or stimulant intake) were also evaluated in terms of the gut microbiota profile. Participants (n 120) underwent anthropometric, dietary, physical activity and lifestyle evaluation. Adherence to the Mediterranean diet was assessed using a Mediterranean diet score, the MedDietScore, and subjects were classified into three tertiles according to individual adherence scoring. Gut microbiota composition was determined using quantitative PCR and plate-count techniques, and faecal SCFA were analysed using GC. Gastrointestinal symptoms were also evaluated. Participants with a high adherence to the Mediterranean diet had lower Escherichia coli counts (P=0·022), a higher bifidobacteria:E. coli ratio (P=0·025), increased levels and prevalence of Candida albicans (P=0·039 and P=0·050, respectively), greater molar ratio of acetate (P=0·009), higher defaecation frequency (P=0·028) and a more pronounced gastrointestinal symptomatology compared with those reporting low adherence. A lower molar ratio of valerate was also observed in the case of high adherence to the Mediterranean diet compared with the other two tertiles (Pfor trend=0·005). Positive correlations of MedDietScore with gastrointestinal symptoms, faecal moisture, total bacteria, bifidobacteria:E. coli ratio, relative share of Bacteroides, C. albicans and total SCFA, as well as negative associations with cultivable E. coli levels and valerate were indicated. Fast food consumption was characterised by suppressed representation of lactobacilli and butyrate-producing bacteria. In conclusion, our findings support a link between adherence to the Mediterranean diet and gut microbiota characteristics.

Mandatory I fortification in bread was introduced in Australia in 2009 in response to the re-emergence of biochemical I deficiency based on median urinary I concentration (UIC)<100 µg/l. Data on the I status of lactating mothers and their infants in Australia are scarce. The primary aim of this study was to assess the I status, determined by UIC and breast milk I concentration (BMIC), of breast-feeding mothers in South Australia and UIC of their infants. The secondary aim was to assess the relationship between the I status of mothers and their infants. The median UIC of the mothers (n 686) was 125 (interquartile range (IQR) 76–200) µg/l and median BMIC (n 538) was 127 (IQR 84–184) µg/l. In all, 38 and 36 % of the mothers had a UIC and BMIC below 100 µg/l, respectively. The median UIC of infants (n 628) was 198 (IQR 121–296) µg/l, and 17 % had UIC<100 µg/l. Infant UIC was positively associated with maternal UIC (β 0·26; 95 % CI 0·14, 0·37, P<0·001) and BMIC (β 0·85; 95 % CI 0·66, 1·04, P<0·001) at 3 months postpartum after adjustment for gestational age, parity, maternal secondary and further education, BMI category and infant feeding mode. The adjusted OR for infant UIC<100 µg/l was 6·49 (95 % CI 3·80, 11·08, P<0·001) in mothers with BMIC<100 µg/l compared with those with BMIC≥100 µg/l. The I status of mothers and breast-fed infants in South Australia, following mandatory I fortification, is indicative of I sufficiency. BMIC<100 µg/l increased the risk of biochemical I deficiency in breast-fed infants.

The aim of the present study was to investigate the relationship of four TNF-α SNP with inflammatory biomarkers and plasma fatty acids (FA), and the interaction among them in a population-based, cross-sectional study in São Paulo, Brazil. A total of 281 subjects, aged >19 and <60 years, participated in a cross-sectional, population-based study performed in Brazil. The following SNP spanning the TNF-α gene were genotyped: -238G/A (rs361525), -308G/A (rs1800629), -857C/T (rs1799724) and -1031T/C (rs1799964). In all, eleven plasma inflammatory biomarkers and plasma FA profile were determined. To analyse the interaction between TNF-α SNP and plasma FA, a cluster analysis was performed to stratify individuals based on eleven inflammatory biomarkers into two groups used as outcome: inflammatory (INF) and non-inflammatory clusters. The -238A allele carriers had higher TNF-α (P=0·033), IL-6 (P=0·013), IL-1β (P=0·037), IL-12 (0·048) and IL-10 (P=0·010) than the GG genotype. The -308A allele carriers also had lower levels of plasma palmitoleic acid (P=0·009), oleic acid (P=0·039), total MUFA (P=0·014), stearoyl-CoA desaturase (SCD) activity index-16 (P=0·007), SCD-18 (P=0·020) and higher levels of PUFA (P=0·046) and DHA (P=0·044). Significant interactions modifying the risk of belonging to the INF cluster were observed with inflammatory cluster as outcome between -857C/T and plasma α-linolenic acid (P=0·026), and also between -308G/A and plasma stearic acid (P=0·044) and total SFA (P=0·040). Our study contributes to knowledge on TNF-α SNP and their association with inflammatory biomarker levels, plasma FA and the interaction among them, of particular interest for the Brazilian population.

Only a few studies have focused on the association between overall diet, rather than intakes of individual nutrients or foods, and depressive symptoms in Japanese. This cross-sectional study examined associations between a diet quality score and depressive symptoms in 3963 young (age 18 years) and 3833 middle-aged (mean age 47·9 (sd 4·2) years) Japanese women. Dietary information was collected using a diet history questionnaire. A previously developed diet quality score was computed mainly based on the Japanese Food Guide Spinning Top. The prevalence of depressive symptoms was 22·0 % for young women and 16·8 % for middle-aged women, assessed as a Center for Epidemiologic Studies Depression (CES-D) score ≥23 and ≥19, respectively. As expected, the diet quality score was associated positively with intakes of ‘grain dishes’, ‘vegetable dishes’, ‘fish and meat dishes’, ‘milk’ and ‘fruits’ and inversely with intakes of energy from ‘snacks, confection and beverages’ and Na from seasonings. After adjustment for potential confounders, OR for depressive symptoms in the highest v. lowest quintiles of the diet quality score was 0·65 (95 % CI 0·50, 0·84) in young women (Pfor trend=0·0005). In middle-aged women, the corresponding value was 0·59 (95 % CI 0·45, 0·78) (Pfor trend<0·0001). Analyses where the diet quality and CES-D scores were treated as continuous variables also showed inverse associations. In conclusion, this cross-sectional study showed that a higher diet quality score was associated with a lower prevalence of depressive symptoms in young and middle-aged Japanese women. Prospective studies are needed to confirm a public health relevance of this finding.

Seafood intake in pregnancy has been positively associated with childhood cognitive outcomes which could potentially relate to the high vitamin D content of oily fish. However, whether higher maternal vitamin D status (serum 25-hydroxyvitamin D (25(OH)D)) in pregnancy is associated with a reduced risk of offspring suboptimal neurodevelopmental outcomes is unclear. A total of 7065 mother–child pairs were studied from the Avon Longitudinal Study of Parents and Children cohort who had data for both serum total 25(OH)D concentration in pregnancy and at least one measure of offspring neurodevelopment (pre-school development at 6–42 months; ‘Strengths and Difficulties Questionnaire’ scores at 7 years; intelligence quotient (IQ) at 8 years; reading ability at 9 years). After adjustment for confounders, children of vitamin D-deficient mothers (<50·0 nmol/l) were more likely to have scores in the lowest quartile for gross-motor development at 30 months (OR 1·20; 95 % CI 1·03, 1·40), fine-motor development at 30 months (OR 1·23; 95 % CI 1·05, 1·44) and social development at 42 months (OR 1·20; 95 % CI 1·01, 1·41) than vitamin D-sufficient mothers (≥50·0 nmol/l). No associations were found with neurodevelopmental outcomes, including IQ, measured at older ages. However, our results suggest that deficient maternal vitamin D status in pregnancy may have adverse effects on some measures of motor and social development in children under 4 years. Prevention of vitamin D deficiency may be important for preventing suboptimal development in the first 4 years of life.

There are limited data on the association between Fe overload and leucocyte telomere length (LTL), known as a useful biomarker of the replicative ageing of cells. The aim of the study was to evaluate associations between Fe-status biomarkers and LTL. A cross-sectional study included 1174 men and women aged 50–79 years who provided blood samples for assays of Fe-status biomarkers including ferritin, transferrin saturation (TSAT), total Fe-binding capacity (TIBC) and relative LTL. They were free of hepatitis, potential infection or Fe deficiency. In multiple linear regression analysis adjusted for potential confounding variables, log-transformed LTL was positively associated with TIBC (adjusted coefficient estimate for its highest quartile: 0·17 (se 0·03), P<0·001) and inversely associated with TSAT (adjusted coefficient estimate for its third and fourth quartiles: −0·09 (se 0·03), P<0·01). These associations were consistent after additional adjustment for serum concentrations of high-sensitivity C-reactive protein, alanine transaminase and aspartate transaminase. In particular, participants with not only abnormally high concentrations (>45 %) but also with high-normal concentrations (35–45 %) of TSAT had shorter LTL compared with those with low-normal concentrations (<30 %) (P<0·05). We also observed that less-active or obese persons with high TSAT concentrations had shorter LTL than others. Our findings that cellular ageing is influenced not only by Fe overload but also by high-normal concentrations of TSAT support the hypothesis regarding the detrimental effects of labile Fe, which has a potent pro-oxidant activity in the body.

Early life nutrition and feeding practices are important modifiable determinants of subsequent obesity, yet little is known about the circadian feeding pattern of 12-month-old infants. We aimed to describe the 24-h feeding patterns of 12-month-old infants and examine their associations with maternal and infant characteristics. Mothers from a prospective birth cohort study (n 431) reported dietary intakes of their 12-month-old infants and respective feeding times using 24-h dietary recall. Based on their feeding times, infants were classified into post-midnight (00.00–05.59 hours) and pre-midnight (06.00–23.59 hours) feeders. Mean daily energy intake was 3234 (sd 950) kJ (773 (sd 227) kcal), comprising 51·8 (sd 7·8) % carbohydrate, 33·9 (sd 7·2) % fat and 14·4 (sd 3·2) % protein. Mean hourly energy intake and proportion of infants fed were lower during post-midnight than pre-midnight hours. There were 251 (58·2 %) pre-midnight and 180 (41·8 %) post-midnight feeders. Post-midnight feeders consumed higher daily energy, carbohydrate, fat and protein intakes than pre-midnight feeders (all P<0·001). The difference in energy intake originated from energy content consumed during the post-midnight period. Majority (n 173) of post-midnight feeders consumed formula milk during the post-midnight period. Using multivariate logistic regression with confounder adjustment, exclusively breast-feeding during the first 6 months of life was negatively associated with post-midnight feeding at 12 months (adjusted OR 0·31; 95 % CI 0·11, 0·82). This study provides new insights into the circadian pattern of energy intake during infancy. Our findings indicated that the timing of feeding at 12 months was associated with daily energy and macronutrient intakes, and feeding mode during early infancy.