Abstract
BACKGROUND: Hydrogen sulfide (H(2)S) is a toxic end-product of microbial fermentation produced in the colon that may play a role in the pathogenesis of several diseases, including ulcerative colitis and colon cancer. However, the effect of diet interventions on intestinal burden of H(2)S gas exposure remains poorly understood. OBJECTIVE: Determine the effect of short-term (1-week) plant- and animal-based eating patterns on ex vivo fecal H(2)S production in healthy human volunteers. METHODS: The study design was an open-label, cross-over diet study and diets were self-administered. Each participant consumed two interventional diets: 1) an animal-based, low fiber (i.e. western) diet and 2) a plant-based, high fiber diet, separated by a two-week washout period. Participants collected full stool samples at the end of each week, which were processed within 2 h of collection to capture H(2)S production. Microfluidic qPCR (MFQPCR) was used to simultaneously quantify multiple taxonomic and functional groups involved in sulfate reduction and the fecal microbiota was characterized through high-throughput DNA sequencing. RESULTS: Median H(2)S production was higher following the animal-based diet compared to the plant-based diet (p = 0.02; median difference 29 ppm/g, 95% CI 16-97). However, there was substantial individual variability and 2 of 11 individuals (18%) produced more H(2)S on the plant-based diet. Using the top and bottom quartiles of H(2)S percent change between animal- and plant-based diet weeks to define responders and non-responders, significant taxonomic differences were observed between the responder and non-responder cohorts. CONCLUSIONS: Here we report that substrate changes associated with a 1-week plant-based diet intervention resulted in lower ex vivo H(2)S production compared to a 1-week animal-based diet intervention in most healthy individuals. However, H(2)S responsiveness to diet was not uniform across the entire cohort, and potential H(2)S production enterotypes were characterized that may predict individualized H(2)S responsiveness to diet.