Psychosocial adversity experienced in utero and early life is associated with variation in gut microbiota: a prospective case-control study

Abstract

AbstractSocial disadvantage (SD) and psychological stressors (PS) trap some populations in poverty, resulting in health inequities. How these two factors become biologically embedded and the pathways leading to adverse health outcomes is unclear, especially in infants exposed to psychosocial adversity in utero and during early life. Variation in gut microbiome structure and functions, and systemic elevations in circulating cytokines levels as indices of inflammation, offer two possible causative pathways. Here, we interrogate the gut microbiome of mother-child dyads and maternal inflammatory markers, and compare high-SD/high-PS dyads to pairs with low-SD/Low-PS, and demonstrate that the GM of high-SD and high-PS mothers may already be compromised, resulting in the lowest observed inter-individual similarity in that group. The strong predictors of maternal high-SD and high-PS based on mothers and children microbiomes were phylogenetically very distinct bacteria indicating different GM pathways associated with SD versus PS. We identified sets of SD- and PS-discriminatory metabolic pathways in the mothers and in the children, however their predictive power was lower compared to the discriminatory bacterial species. Prediction accuracy was consistently greater for IL-6 than for the other inflammatory markers, supporting an association between systemic inflammation and psychosocial adversity. The gut microbiome of the infants can be used to predict the psychosocial adversity of mothers, and are embedded in the gut microbiota of 4-month-old infants.