BMC Microbiol. 2025 Jul 19;25(1):442. doi: 10.1186/s12866-025-04146-6.
ABSTRACT
BACKGROUND: The perinatal period has been linked with higher vulnerability to stress and symptoms of depression and anxiety, as well as with dynamic changes in the composition of maternal gut microbiota. While recent studies indicated significant associations between stress, depression, or anxiety, and alterations in gut microbiota in pregnant women, research in this avenue is still emerging, with existing studies often being limited by small sample sizes.
METHOD: We conducted a prospective longitudinal study of 171 women, collecting gut microbiota samples in each trimester of pregnancy and in the early postpartum, questionnaire data (perceived stress via the Perceived Stress Scale, symptoms of depression via the Edinburgh Postnatal Depression Scale, and anxiety via the 6-item State-Trait Anxiety Inventory) twice in each trimester and twice in the early postpartum period, and blood samples for cortisol levels analysis in the first and third pregnancy trimesters. Gut microbiota samples were analyzed by amplicon sequencing of 16S rRNA gene.
RESULTS: Perceived stress and symptoms of depression and anxiety showed moderate temporal changes and a high consistency at the individual level over the study period. Cortisol levels rose significantly from the first to the third trimester. There were significant temporal changes in microbiota composition between the first and second trimesters, and between the first and third trimesters. After controlling for false positive findings due to multiple testing, we found no significant associations between stress-related variables (perceived stress, cortisol levels, symptoms of depression and anxiety) and gut microbiota diversity, microbial community composition, or relative abundances of individual bacterial taxa.
CONCLUSIONS: The present study results contradict previous research that indicated significant associations between emotions and gut microbiota in the perinatal period. Although we cannot provide an ultimate explanation for this discrepancy, we propose it can lie in insufficient control for false positives in the differential abundance analyses in most previous studies.
PMID:40684088 | DOI:10.1186/s12866-025-04146-6
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