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Background Early introduction of complementary foods has been associated with various immune disorders, oxidative stress, and obesity in childhood. The gut microbiota and the short chain fatty acids (SCFAs) they produce are postulated to be on the causal pathway. The objective of this study was to determine if early complementary feeding (i.e. consumption of solids or non-water/formula liquids at or before 3 months) is prospectively associated with infant gut microbiota composition, diversity and SCFAs at 3 and 12 months of age in the Nurture birth cohort. Results Mother-infant dyads in the early complementary feeding group ( n  = 18) had similar baseline characteristics to those in the later feeding group ( n  = 49). We assessed differential abundance of microbial taxa (measured by 16S rRNA gene sequencing of the V4 region) by timing of complementary feeding using beta-binomial regression models (considering a two-sided FDR corrected p -value of < 0.05 as significant), and we fittted linear regression models to assess the association between early complementary feeding and SCFA concentrations (quantified using gas chromatography). After multivariable adjustment for breastfeeding, delivery method, birth weight, and gestational age, there were 13 differentially abundant microbial amplicon sequence variants (ASVs) by timing of introduction to complementary foods at 3 months and 20 ASVs at 12 months. Infants introduced to complementary foods early (vs. later) had higher concentrations of the SCFA butyric acid (mean difference = 0.65, 95% CI: 0.27, 1.04, p  < 0.01) and total SCFAs (mean difference = 38.8, 95% CI: 7.83, 69.7) at 12 months. Bilophila wadsworthia and Lachnospiraceae Roseburia were associated with early (vs. later) complementary feeding and with higher butyric acid concentrations at 3 and 12 months, respectively. Conclusions Our findings are consistent with the hypothesis that early (vs. later) introduction to complementary foods is associated with altered gut microbiota composition and butyric acid concentrations measured in stool until at least 1 year of age. Further research is needed to determine if these changes mediate future development of metabolic and immune conditions.

Children delivered by elective C-section are not exposed to the birth canal and show altered microbiota development. Impairing microbial colonization during early life alters metabolic and immune programming and is associated with an increased risk of immune and metabolic diseases. Children delivered by elective, prelabor Cesarean section (C-section) are not exposed to the birth canal microbiota and, in relation to vaginally delivered children, show altered microbiota development. Perturbed microbial colonization during critical early-life windows of development alters metabolic and immune programming and is associated with an increased risk of immune and metabolic diseases. In nonrandomized studies, vaginal seeding of C-section-born neonates partially restores their microbiota colonization to that of their vaginally delivered counterparts, but without randomization, confounding factors cannot be excluded. In a double-blind, randomized, placebo-controlled trial, we determined the effect of vaginal seeding versus placebo seeding (control arm) on the skin and stool microbiota of elective, prelabor C-section-born neonates ( n  = 20) at 1 day and 1 month after birth. We also examined whether there were between-arm differences in engraftment of maternal microbes in the neonatal microbiota. In relation to the control arm, vaginal seeding increased mother-to-neonate microbiota transmission and caused compositional changes and a reduction in alpha diversity (Shannon Index) of the skin and stool microbiota. The neonatal skin and stool microbiota alpha diversity when maternal vaginal microbiota is provided is intriguing and highlights the need of larger randomized studies to determine the ecological mechanisms and effects of vaginal seeding on clinical outcomes. IMPORTANCE Children delivered by elective C-section are not exposed to the birth canal and show altered microbiota development. Impairing microbial colonization during early life alters metabolic and immune programming and is associated with an increased risk of immune and metabolic diseases. In a double-blind, randomized, placebo-controlled trial, we determined the effect of vaginal seeding on the skin and stool microbiota of elective C-section born neonates and found that vaginal seeding increased mother-to-neonate microbiota transmission and caused compositional changes and a reduction in the skin and stool microbiota diversity. The reduction of neonatal skin and stool microbiota diversity when maternal vaginal microbiota is provided is intriguing and highlights the need of larger randomized studies to determine the ecological mechanisms and effects of vaginal seeding on clinical outcomes.

Background Prenatal antibiotic exposure has been associated with an altered infant gut microbiome composition and higher risk of childhood obesity, but no studies have examined if prenatal antibiotics simultaneously alter the gut microbiome and adiposity in infants. Method In this prospective study (Nurture: recruitment 2013–2015 in North Carolina, United States), we examined in 454 infants the association of prenatal antibiotic exposure (by any prenatal antibiotic exposure; by trimester of pregnancy; by number of courses; by type of antibiotics) with infant age- and sex-specific weight-for-length z score (WFL-z) and skinfold thicknesses (subscapular, triceps, abdominal) at 12 months of age. In a subsample, we also examined whether prenatal antibiotic exposure was associated with alterations in the infant gut microbiome at ages 3 and 12 months. Results Compared to infants not exposed to prenatal antibiotics, infants who were exposed to any prenatal antibiotics had 0.21 (95% confidence interval [CI] 0.02, 0.41) higher WFL-z at 12 months, and 0.28 (95% CI 0.02, 0.55) higher WFL-z if they were exposed to antibiotics in the second trimester, after adjustment for potential confounders, birth weight, and gestational age. We also observed a dose-dependent association (P-value for trend = 0.006) with infants exposed to ≥ 3 courses having 0.41 (95% CI 0.13, 0.68) higher WFL-z at 12 months. After further adjustment for delivery method, only second-trimester antibiotic exposure remained associated with higher infant WFL-z (0.27, 95% CI 0.003, 0.54) and subscapular skinfold thickness (0.49 mm, 95% CI 0.11, 0.88) at 12 months. Infants exposed to second-trimester antibiotics versus not had differential abundance of 13 bacterial amplicon sequence variants (ASVs) at age 3 months and 17 ASVs at 12 months (false discovery rate adjusted P-value < 0.05). Conclusions Prenatal antibiotic exposure in the second trimester was associated with an altered infant gut microbiome composition at 3 and 12 months and with higher infant WFL-z and subscapular skinfold thickness at 12 months.

Differding and Mueller cite that the prevalence of childhood obesity continues to rise globally, making it more important than ever to identify modifiable risk factors for prevention. High use of disinfectants has been shown to reduce household presence of microbes and to alter the microbiome in piglets; endocrine-disrupting agents present in many products are capable of negatively affecting child growth. New research has examined associations between household cleaning agents, the microbiome at three to four months and childhood obesity, finding an association between high disinfectant use and obesity that may be partly mediated by Lachnospiraceae. Although these associations are biologically plausible, further research is needed to understand whether residual confounding might have accounted for current findings, and to provide stronger evidence on whether endocrine-disrupting agents in antimicrobial cleaners are obesogenic.

Background/Objectives: Murine models show that plastics, via their chemical constituents (e.g., phthalates), influence microbiota, metabolism, and growth. However, research on plastics in humans is lacking. Here, we examine how the frequency of plastic bottle exposure is associated with fecal microbiota, short-chain fatty acids (SCFAs), and anthropometry in the first year of life. Subjects/Methods: In 442 infants from the prospective Nurture birth cohort, we examined the association of frequency of plastic bottle feeding at 3 months with anthropometric outcomes (skinfolds, length-for-age, and weight-for-length) at 12 months of age and growth trajectories between 3 and 12 months. Furthermore, in a subset of infants (n = 70) that contributed fecal samples at 3 months and 12 months of age, we examined plastic bottle frequency in relation to fecal microbiota composition and diversity (measured by 16S rRNA gene sequencing of V4 region), and fecal SCFA concentrations (quantified using gas chromatography mass spectrometry). Results: At 3 months, 67.6% of infants were plastic bottle fed at every feeding, 15.4% were exclusively breast milk fed, and 48.9% were exclusively formula fed. After adjustment for potential confounders, infants who were plastic bottle fed less than every feeding compared to those who were plastic bottle fed at every feeding at 3 months did not show differences in anthropometry over the first 12 months of life, save for lower length-for-age z-score at 12 months (adjusted β = −0.45, 95% CI: −0.76, −0.13). Infants who were plastic bottle fed less than every feeding versus every feeding had lower fecal microbiota alpha diversity at 3 months (mean difference for Shannon index: −0.59, 95% CI: −0.99, −0.20) and lower isovaleric acid concentration at 3 months (mean difference: −2.12 μmol/g, 95% CI: −3.64, −0.60), but these results were attenuated following adjustment for infant diet. Plastic bottle frequency was not strongly associated with microbiota diversity or SCFAs at 12 months after multivariable adjustment. Frequency of plastic bottle use was associated with differential abundance of some bacterial taxa, however, significance was not consistent between statistical approaches. Conclusions: Plastic bottle frequency at 3 months was not strongly associated with measures of adiposity or growth (save for length-for-age) over the first year of life, and while plastic bottle use was associated with some features of fecal microbiota and SCFAs in the first year, these findings were attenuated in multivariable models with infant diet. Future research is needed to assess health effects of exposure to other plastic-based products and objective measures of microplastics and plastic constituents like phthalates.

Background Maternal pre-pregnancy body mass index (BMI) has been linked to altered gut microbiota in women shortly after delivery and in their offspring in the first few years of life. But little is known about how long these differences persist. Methods We followed 180 mothers and children from pregnancy until 5-year postpartum in the Gen3G cohort (Canada, enrolled 2010–2013). At 5 years postpartum we collected stool samples from mothers and children and estimated the gut microbiota by 16 S rRNA sequencing (V4 region) using Illumina MiSeq, and assigning amplicon sequence variants (ASV). We examined whether overall microbiota composition (as measured by microbiota β diversity) was more similar between mother-child pairs compared to between mothers or between children. We also assessed whether mother-child pair sharing of overall microbiota composition differed by the weight status of mothers before pregnancy and of children at 5-year. Furthermore, in mothers, we examined whether pre-pregnancy BMI, BMI 5-year postpartum, and change in BMI between time points was associated with maternal gut microbiota 5-year postpartum. In children, we further examined associations of maternal pre-pregnancy BMI and child 5-year BMI z-score with child 5-year gut microbiota. Results Mother-child pairs had greater similarity in overall microbiome composition compared to between mothers and between children. In mothers, higher pre-pregnancy BMI and 5-year postpartum BMI were associated with lower microbiota observed ASV richness and Chao 1 index; in children’s gut microbiota, higher maternal pre-pregnancy BMI was weakly associated with lower microbiota Shannon index, whereas child’s 5-year BMI z-score was associated with higher observed ASV richness. Pre-pregnancy BMI was also linked to differential abundances of several microbial ASVs in the Ruminococcaceae and Lachnospiraceae families, but no specific ASV had overlapping associations with BMI measures in both mothers and children. Conclusions Pre-pregnancy BMI was associated with gut microbiota diversity and composition of mothers and children 5 years after birth, however, the nature and direction of most associations differed for mothers and children. Future studies are encouraged to confirm our findings and look into potential mechanisms or factors that may drive these associations.