The Rationale for Sulforaphane Favourably Influencing Gut Homeostasis and Gut-Organ Dysfunction: A Clinician's Hypothesis

Int J Mol Sci. 2023 Aug 30;24(17):13448. doi: 10.3390/ijms241713448.

Abstract

Given the increasing scientific, clinical and consumer interest in highly prevalent functional gastrointestinal disorders, appropriate therapeutic strategies are needed to address the many aspects of digestive dysfunction. Accumulating evidence for the crucifer-derived bioactive molecule sulforaphane in upstream cellular defence mechanisms highlights its potential as a therapeutic candidate in targeting functional gastrointestinal conditions, as well as systemic disorders. This article catalogues the evolution of and rationale for a hypothesis that multifunctional sulforaphane can be utilised as the initial step in restoring the ecology of the gut ecosystem; it can do this primarily by targeting the functions of intestinal epithelial cells. A growing body of work has identified the colonocyte as the driver of dysbiosis, such that targeting gut epithelial function could provide an alternative to targeting the microbes themselves for the remediation of microbial dysbiosis. The hypothesis discussed herein has evolved over several years and is supported by case studies showing the application of sulforaphane in gastrointestinal disorders, related food intolerance, and several systemic conditions. To the best of our knowledge, this is the first time the effects of sulforaphane have been reported in a clinical environment, with several of its key properties within the gut ecosystem appearing to be related to its nutrigenomic effects on gene expression.

Keywords: chronic disease; dysbiosis; epithelium; food intolerance; gut barrier; gut ecology; gut–organ axis; microbiome; nutrigenomics; nutritional medicine; sulforaphane.

MeSH terms

  • Dysbiosis* / drug therapy
  • Ecosystem*
  • Homeostasis
  • Humans
  • Multiple Organ Failure

Substances

  • sulforaphane

Grants and funding

This research received no external funding.