Human milk is considered the optimal nutrition for infants and found to contain significant numbers of viable bacteria. The aim of the study was to assess the effects of a specific synbiotic combination at doses closer to the bacterial cells present in human milk, on intestinal bifidobacteria proportions (relative abundance), reduction of potential pathogens and gut physiological conditions. A clinical study was conducted in 290 healthy infants aged from 6 to 19 weeks. Infants received either a control infant formula or one of the two investigational infant formulas (control formula with 0.8 g/100 ml scGOS/lcFOS and Bifidobacterium breve M-16V at either 1 × 104 cfu/ml or 1 × 106 cfu/ml). Exclusively breastfed infants were included as a reference. Analyses were performed on intention-to-treat groups and all-subjects-treated groups. After 6 weeks of intervention, the synbiotics at two different doses significantly increased the bifidobacteria proportions in healthy infants. The synbiotic supplementation also decreased the prevalence (infants with detectable levels) and the abundance of C. difficile. Closer to the levels in the breastfed reference group, fecal pH was significantly lower while l-lactate concentrations and acetate proportions were significantly higher in the synbiotic groups. All formulas were well tolerated and all groups showed a comparable safety profile based on the number and severity of adverse events and growth. In healthy infants, supplementation of infant-type bifidobacterial strain B. breve M-16V, at a dose close to bacterial numbers found in human milk, with scGOS/lcFOS (9:1) created a gut environment closer to the breastfed reference group. This specific synbiotic mixture may also support gut microbiota resilience during early life.Clinical Trial Registration This clinical study named Color Synbiotics Study, was registered in ClinicalTrials.gov on 18 March 2013. Registration number is NCT01813175. https://clinicaltrials.gov/ct2/show/NCT01813175.

Background Age, race, and analytic method influence levels of blood amino acids, of which reference intervals are required for the diagnosis and management of inherited metabolic disorders. Objectives To establish age-specific reference intervals for blood amino acids in Thai pediatric population measured by liquid chromatography tandem mass spectrometry (LC-MS/MS). Methods A cross-sectional study of 277 healthy children from birth to 12 years was conducted. Anthropometric, clinical, and dietary information were recorded. Dried blood spots on a filtered paper were used for measurement by derivatized LC-MS/MS. Factors that might affect amino acids such as fasting time and dietary intake were analyzed using quantile regression analysis. Results Levels of thirteen blood amino acids were reported as median and interval from 2.5th–97.5th percentiles. Compared with those of Caucasian, most blood amino acid levels of Thai children were higher. Compared with a previous study using HPLC in Thai children, many amino acid levels are different. Glycine, alanine, leucine/isoleucine, and glutamic acid sharply decreased after birth. Citrulline, arginine, and methionine stayed low from birth throughout childhood, whereas phenylalanine was at middle level and slightly increased during preadolescence. Conclusion Reference intervals of age-specific blood amino acids using LC-MS/MS were established in the Thai pediatric population. They diverge from previous studies, substantiating the recommendation that, for the optimal clinical practice, age-specific reference intervals of amino acids should be designated for the particular population and analysis method.

Introduction. Iron deficiency (ID) is the most common nutritional deficiency found in pediatric practice. A higher prevalence of ID may be found in children with obesity. Obesity is a chronic low-grade inflammatory condition. It is postulated that inflammation increases hepcidin, a regulator of iron homeostasis. The aim of this study was to investigate the associations between iron status, hepcidin, and BMI-standard deviation score (BMI-SDS) in children with and without obesity. Methods. A cross-sectional study of Thai children with obesity (5 to 15 years old) versus age- and sex-matched, nonobese controls was conducted. A total of 63 children with obesity and 27 controls were enrolled. Complete blood count, serum iron, ferritin, transferrin saturation, and total iron binding capacity were analyzed. Serum hepcidin-25 was assayed using a hepcidin ELISA Kit (Human Hepc25). Results. There were 63 children with obesity, the median age (IQR) being 10 (9–13) years, and 27 controls. The median (IQR) BMI-SDS of the obese group was 2.3 (2.0–2.6) vs. −0.5 ((−1.3)−0.4) of the control group. ID was diagnosed in 27 children in the obese group (42.9%); 4 of the children with obesity and ID had anemia. Serum hepcidin-25 levels of the children with ID vs. without ID in the obese group were not significantly different (median (IQR) 25 (12.9–49.2) and 26.4 (12.6–43.6), respectively) but both of them were significantly higher than controls (19.7 (8.3–25.5) ng/ml, p  = 0.04). BMI-SDS was positively correlated with hepcidin-25 (r = 0.28, p  = 0.001). Conclusion. Prevalence of iron deficiency in Thai children with obesity and serum hepcidin-25 was higher than controls. Further study in a larger population, preferably with interventions such as weight loss program, is warranted to clarify this association.