DIET AND MICROBIOME INTERACTIONS: ASSOCIATIONS IN POSTTRAUMATIC STRESS DISORDER (D-MAPS)

Abstract

Posttraumatic Stress Disorder (PTSD) is a mental health disorder that develops after an individual experiences or witnesses a traumatic event. People with PTSD often have higher levels of inflammation potentially mediated by the gut microbiome. Current research suggests that increased gut microbial diversity reduces inflammation and inflammation-associated conditions. Specifically, the “Old Friends” hypothesis suggests that humans co-evolved with an extremely diverse microbial ecosystem that interacts with our immune system to protect against pathogenic microbes and inflammatory conditions through direct effects in the gut, as well as systemically, via the Gut-Brain-Immune axis. These microbes are influenced by our diets and lifestyles, and over time, the amount and diversity of plant-based foods in human diets have decreased. As a result, we have lost some of these “old friends” from the gut microbiota. Here, I review literature related to the “old friends” hypothesis and the interactions between the gut and brain (Chapter 1), describe a parallel arm, randomized controlled clinical intervention study protocol designed as a pilot study to test the impact of increasing plant diet diversity on gut microbial diversity, PTSD symptoms, and inflammation (Chapter 2), and describe the microbial communities of test beverages for the study (Chapter 3). Results for Chapter 2 have yet to be determined as the clinical study is still under way. Results from Chapter 3 revealed higher microbial diversity in the high plant diversity treatment beverage (30 plants) compared to the low plant diversity treatment beverage (3 plants). Both treatment beverage microbiomes were stable under refrigerated conditions (4°C) for four weeks.The long-term objective is to test the hypothesis that daily consumption of a high plant diversity beverage will increase microbial diversity in the gut-microbiome of people with diagnosed PTSD, improve PTSD symptoms, and lower levels of inflammation-associated biomarkers. This work lays the foundation for pursuing this hypothesis.