Dietary factors in sulfur metabolism and pathogenesis of ulcerative colitis

Levi M. Teigen, Zhuo Geng, Michael J Sadowsky, Byron P Vaughn, Matthew J Hamilton, Alexander Khoruts

Research output: Contribution to journalReview articlepeer-review

28 Scopus citations


The biogeography of inflammation in ulcerative colitis (UC) suggests a proximal to distal concentration gradient of a toxin. Hydrogen sulfide (H2S) has long been considered one such toxin candidate, and dietary sulfur along with the abundance of sulfate reducing bacteria (SRB) were considered the primary determinants of H2S production and clinical course of UC. The metabolic milieu in the lumen of the colon, however, is the result of a multitude of factors beyond dietary sulfur intake and SRB abundance. Here we present an updated formulation of the H2S toxin hypothesis for UC pathogenesis, which strives to incorporate the interdependency of diet composition and the metabolic activity of the entire colon microbial community. Specifically, we suggest that the increasing severity of inflammation along the proximal-to-distal axis in UC is due to the dilution of beneficial factors, concentration of toxic factors, and changing detoxification capacity of the host, all of which are intimately linked to the nutrient flow from the diet.

Original languageEnglish (US)
Article number931
Issue number4
StatePublished - Apr 2019

Bibliographical note

Funding Information:
Acknowledgments: This work was partially supported by grants from the Healthy Foods Healthy Lives Institute, the Allen Foundation, and Achieving Cures Together.

Funding Information:
Conflicts of Interest: B.P.V. has received compensation from speaking and/or ad boards from Abbvie and Janssen and has received grant support from Roche, Takeda, Celgene and Diasorin.

Publisher Copyright:
© 2019 by the authors. Licensee MDPI, Basel, Switzerland.

Copyright 2019 Elsevier B.V., All rights reserved.


  • Colon
  • High-sulfur foods
  • Inflammation
  • Metagenomics
  • Microbiota
  • Sulfur reducing


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