The author of this 2023 paper expanded Part 1 to include further clinical evidence and four human case studies. I’ll highlight just a few items because it’s quite detailed:
“Accumulating evidence for the crucifer-derived bioactive molecule sulforaphane (SFN) 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 evolution of and rationale for a hypothesis that multifunctional sulforaphane can be utilised as the initial step in restoring ecology of the gut ecosystem.
It can do this primarily by targeting functions of intestinal epithelial cells. In many cases where primary presenting symptoms are related to aberrant intestinal function, complete or partial resolution also occurred in seemingly unrelated conditions such as inflammatory skin diseases, multiple food intolerances, histamine-like allergic reactions, and neuro-psychological disorders.
Although SFN was the primary and initial intervention, clinicians recommended that their patients consume a mixed diet of minimally processed foods rich in vegetables and other sources of phytochemicals. It was also clear that dietary recommendations alone were not capable of making changes that occurred when SFN was added.

In seeking an effective gateway for addressing digestive, immune, cardiometabolic and other chronic disease, this hypothesis proposes an approach that harnesses the endogenous processes of human cells. These processes focus on restoring homeostasis to the gut, its underlying immune network, and the companion microbiota, with the collective potential to beneficially impact all gut–organ axes.”
https://www.mdpi.com/1422-0067/24/17/13448 “The Rationale for Sulforaphane Favourably Influencing Gut Homeostasis and Gut–Organ Dysfunction: A Clinician’s Hypothesis”
The author proposed this paper as a working hypothesis to be scientifically correct. Would a null hypothesis be along the lines of “I’ll eat a clinically relevant dose of broccoli sprouts every day for twelve weeks, and nothing will change”?
Case study #1 had a timing parallel with my experiences per:
“She was able to tolerate 20 mg SFN daily after several weeks; the dose was increased to 40 mg daily by 6 weeks.”
I doubled my dose at Week 6. All case studies documented transformative experiences, but they weren’t the same types that shortly followed for me.
Interesting synergy between zinc and sulforaphane! On a side note, I just recently discovered that much of the sulforaphane we consume is wasted unless we take NQ01 activators or BET protein inhibitors at he same time. During aging NQ01 activity declines, rendering NRF2 activators like sulforaphane useless. For young people, this might not be a problem but for people 50+, it definetely is. SIRT1 is an acitivator of NQ01, as is beta-lapachone. I’ll start combining beta-lapachone with sulforaphane. I already fast everyday, which also acitivates SIRT1. Resveratrol is a potent BET inhibitor, but I don’t have good experience with resveratrol, unfortunately.