Objective Inadequate immunoregulation and elevated inflammation may be risk factors for posttraumatic stress disorder (PTSD), and microbial inputs are important determinants of immunoregulation; however, the association between the gut microbiota and PTSD is unknown. This study investigated the gut microbiome in a South African sample of PTSD-affected individuals and trauma-exposed (TE) controls, to identify potential differences in microbial diversity or microbial community structure. Methods The Clinician Administered Posttraumatic Stress Disorder Scale for DSM-5 (CAPS-5) was used to diagnose PTSD according to DSM-5 criteria. Microbial DNA was extracted from stool samples obtained from 18 individuals with PTSD and 12 TE control participants. Bacterial 16S ribosomal RNA (rRNA) gene V3/V4 amplicons were generated and sequenced. Microbial community structure, alpha-diversity, and beta-diversity were analyzed; random forest analysis was used to identify associations between bacterial taxa and PTSD. Results There were no differences between PTSD and TE control groups in alpha- or beta-diversity measures (e.g., alpha-diversity, Shannon index, t = 0.386, P = .70; beta diversity, based on analysis of similarities (ANOSIM), Bray Curtis test statistic = −0.033, P = .70); however, random forests analysis highlighted three phyla as important to distinguish PTSD status: Actinobacteria, Lentisphaerae, and Verrucomicrobia. Decreased total abundance of these taxa was associated with higher PTSD CAPS scores (r = −.387, P = .035). Conclusions In this exploratory study, measures of overall microbial diversity were similar among individuals with PTSD and TE controls; however, decreased total abundance of Actinobacteria, Lentisphaerae, and Verrucomicrobia was associated with PTSD status.

Global urbanization, combined with evidence of increased prevalence of mental illness in urban environments, highlights a need to investigate potential connections between the built environment and mental health. Previous research has shown that the built environment may impact occupant mental health through its effects on connection to nature, personal control and indoor air quality. Contact with the natural environment has physiological and psychological benefits; consequently, reduced contact or exposure leads to negative mental health outcomes. The control an occupant has in the built environment can alter the mental health of individuals through direct pathways, such as prevention of exposures to environmental stressors and indirect pathways, such as social connections to others. Indoor air quality is connected to the mental health of built environment occupants, as particulate matter, malodorous irritants and toxins have all been shown to alter mental well-being. Opportunities for architects and engineers to optimize building designs that improve occupant mental health include planned urban greenspace, personalized temperature control and building ventilation. To understand optimization targets, interdisciplinary research utilizing controlled experiments are needed to confirm causality and improve our current understanding of mechanisms underlying the association between the built environment and mental health.

The hygiene or “Old Friends” hypothesis proposes that the epidemic of inflammatory disease in modern urban societies stems at least in part from reduced exposure to microbes that normally prime mammalian immunoregulatory circuits and suppress inappropriate inflammation. Such diseases include but are not limited to allergies and asthma; we and others have proposed that the markedly reduced exposure to these old friends in modern urban societies may also increase vulnerability to neurodevelopmental disorders and stress-related psychiatric disorders, such as anxiety and affective disorders, where data are emerging in support of inflammation as a risk factor. Here we review recent advances in our understanding of the potential for old friends, including environmental microbial inputs, to modify risk for inflammatory disease, with a focus on neurodevelopmental and psychiatric conditions. We highlight potential mechanisms, involving bacterially-derived metabolites, bacterial antigens, and helminthic antigens, through which these inputs promote immunoregulation. Though findings are encouraging, significant human subjects research is required to evaluate the potential impact of old friends, including environmental microbial inputs, on biological signatures and clinically meaningful mental health prevention and intervention outcomes.