Social and psychological adversity are associated with distinct mother and infant gut microbiome variationsOriginal paper
What was studied?
This study asked how prenatal social disadvantage and psychosocial stressors relate to the gut microbiome of mothers and their infants. It also linked microbiome features to maternal inflammation. Researchers profiled mother and infant stool using 16S rRNA sequencing and whole metagenomic shotgun sequencing. Machine learning and differential abundance tests identified discriminating taxa. Maternal third-trimester cytokines IL-6, IL-8, IL-10, and TNF-alpha were measured to probe an inflammatory link.
Who was studied?
The cohort was 121 mother-child dyads drawn from the prospective eLABE birth study in St. Louis, USA. Infant stool was collected at 4 months. All 121 dyads had 16S profiling, and 89 selected for extreme exposure scores underwent shotgun metagenomics. Mothers were oversampled for social disadvantage. Infants were term births with almost no antibiotic exposure. Social disadvantage and psychosocial stress were scored as separate latent variables.
What were the most important findings?
Microbiome profiles predicted maternal social disadvantage more accurately than psychosocial stress, reaching 81 to 91 percent accuracy in mothers and children versus about 63 to 69 percent for stress. Many Bifidobacterium species discriminated exposure groups. In infants, the probiotic Bifidobacterium averaged 28.3 percent of the low-disadvantage gut but only 5.2 percent in high-disadvantage infants, tracking reduced breastfeeding. Infant gut genomes predicted high maternal prenatal IL-6 with 66.7 percent accuracy (p = 0.029), overlapping disadvantage-linked taxa.
What are the greatest implications of this study?
The work is the first human study to separate social disadvantage from psychosocial stress in shaping the gut microbiome, showing distinct taxa and pathways for each. Lower breastfeeding among disadvantaged mothers appears to drive infant microbiome differences, supporting policies that expand breastfeeding resources. The authors stress these are associations, not proof of causation, and cytokine analyses used small subsamples requiring validation.