The primary aim of this review was to systematically evaluate the literature regarding the effect of pre-, pro-, or synbiotic supplementation in infant formula on the gastrointestinal microbiota. The Cochrane methodology for systematic reviews of randomized controlled trials (RCTs) was employed. Five databases were searched and 32 RCTs (2010-2021) were identified for inclusion: 20 prebiotic, 6 probiotic, and 6 synbiotic. The methods utilized to evaluate gastrointestinal microbiota varied across studies and included colony plating, fluorescence in situ hybridization, quantitative real-time polymerase chain reaction, or tagged sequencing of the 16S rRNA gene. Fecal Bifidobacterium levels increased with supplementation of prebiotics and synbiotics but not with probiotics alone. Probiotic and synbiotic supplementation generally increased fecal levels of the bacterial strain supplemented in the formula. Across all pre-, pro-, and synbiotic-supplemented formulas, results were inconsistent regarding fecal Clostridium levels. Fecal pH was lower with some prebiotic and synbiotic supplementation; however, no difference was seen with probiotics. Softer stools were often reported in infants supplemented with pre- and synbiotics, yet results were inconsistent for probiotic-supplemented formula. Limited evidence demonstrates that pre- and synbiotic supplementation increases fecal Bifidobacterium levels. Future studies utilizing comprehensive methodologies and additional studies in probiotics and synbiotics are warranted.
Gastrointestinal Microbiome , Probiotics , Synbiotics , Infant , Humans , Prebiotics , Systematic Reviews as Topic , Bifidobacterium
BACKGROUND: Previous research examined effects of human milk on the infant gut microbiota, but little attention has been given to the microbiota of lactating women. RESEARCH AIM: To determine associations between exclusive human milk feeding and gut microbiota characteristics in mothers and infants at 6-weeks postpartum. METHODS: A sample of mother-infant dyads (N = 24) provided fecal samples and questionnaire responses at 6-weeks postpartum as part of the Pregnancy, EAting & POstpartum Diapers study. Deoxyribonucleic acid was extracted from stool samples, followed by (V4) 16S ribosomal ribonucleic acid gene amplicon sequencing. Alpha and beta diversity, in addition to taxa differences, were compared by human milk exposure status, exclusive versus non-exclusive. A subset of dyads (those exclusively fed human milk; n = 14) was analyzed for shared bifidobacterial species using polymerase chain reaction. RESULTS: Alpha diversity was significantly lower in exclusively human milk-fed infants. Maternal lactation status (exclusive vs. partial) and Shannon diversity were associated in univariate analysis but were no longer associated in multivariable regression including body mass index category in the model. Beta diversity (Sorensen dissimilarity) of fecal samples from women and infants was significantly associated with human milk feeding. Of six infants with Bifidobacterium longum subspecies longum in their fecal samples, all their mothers shared the same species. CONCLUSION: Maternal gut microbiotas differ by lactation status, a relationship potentially confounded by body mass index category. Further research is needed to identify whether lactation directly influences the maternal gut microbiota, which may be another mechanism by which lactation influences health.
Breast Feeding , Lactation , Bacteria/genetics , Feces , Female , Humans , Infant , Milk, Human/microbiology , Postpartum Period , Pregnancy
Herein, we report the abundance and prevalence of HMO-metabolizing genes, specifically those of Bifidobacterium infantis, in fecal samples from human infants. Forty dyads were enrolled, and each mother collected a fecal sample from her infant at six months of age. Genomic DNA was extracted, and quantitative real-time PCR was used to determine gene abundance. The mode of delivery was not associated with gene abundance. Several gene regions, Sia (a sialidase), B. inf (16S), and GH750 (a glycoside hydrolase), were more abundant in the feces of human milk-fed infants (p < 0.05). Others, Sia and HC bin (16S), tended to be less abundant when a larger percentage of an infant's diet consisted of solids (p < 0.10). When accounting for solid food intake, human milk exposure was positively associated with Sia and B. inf (p < 0.05) and tended to be related to the abundance of the GH750 and HC bin (p < 0.10) gene regions. With further development and validation in additional populations of infants, these assays could be used to group samples by dietary exposure even where no record of dietary intake exists. Thus, these assays would provide a method by which infant human milk intake can be assessed quickly in any well-equipped molecular biology laboratory.
